Paired lines of C3H mouse fibroblasts transformed with murine sarcoma virus (Kirsten strain) were prepared that express high or low levels ofclass II major histocompatibility complex antigen after treatment with interferon y (IFN-y) . Here, we described a comparison of the tumorigenicity of these lines in euthymic syngeneic and thymus-deficient nu/nu mice and in mice depleted of IFN-y . The class II-inducible cells are clearly less tumorigenic than the noninducible cells in syngeneic mice, but of similar tumorigenicity in nu/nu mice and in mice treated with antibodies to deplete IFN-y . We propose that in this system, IFN-y induction of class II antigens on the tumor cell surface operates to limit tumor growth ; ras expression, which inhibits induction of class II antigens, prevents this and so allows tumor growth .

Looking for Major histocompatability complex? Find out information about Major histocompatability complex. In vertebrates, a family of genes that encode cell surface glycoproteins that regulate interactions among cells of the immune system, some components of the... Explanation of Major histocompatability complex

The first step in the induction of immune responses, whether humoral or cell mediated, requires the interaction between antigen-presenting cells and T lymphocytes restricted at the major histocompatibility complex (MHC). These cells invariably express MHC class II molecules (HLA-D region in man and Ia in mouse) which are recognized by T cells of the helper/inducer subset in association with antigen fragments. Interestingly, in certain pathological conditions, for example in autoimmune diseases such as thyroiditis and diabetic insulitis, class II molecules may be expressed on epithelial cells that normally do not express them. We speculated that these cells may be able to present their surface autoantigens to T cells, and that this process may be crucial to the induction and maintenance of autoimmunity. A critical test of this hypothesis would be to determine whether epithelial cells bearing MHC class II molecules (class II+ cells) can present antigen to T cells. We report here that class II+ thyroid

Clone REA296 recognizes MHC class II-associated invariant chain (Ii)-derived peptide (CLIP) complexes. MHC class II αβ heterodimers associate early during biosynthesis with a type II membrane protein, the invariant chain (Ii). The invariant chain serves as a chaperone for MHC II molecules and mediates trafficking to the endosomal pathway. In the endosomal pathway Ii is sequentially degraded, leaving a residual CLIP in the peptide-binding groove of MHC II. In presence of antigen peptide fragments, HLA-DM then binds to the MHC II molecule, releasing CLIP and allowing peptides to bind. REA296 detects HLA class II-positive cells which have impaired HLA-DM activity, and tumor cells that have escaped immuno-surveillance by CD4-positive T cells.Additional information: Clone REA296 displays negligible binding to Fc receptors. - Belgique

Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments.

Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments.

Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route; where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules; and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments; exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides; autophagosomes constitutively fuse with MHC class II loading ...

Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route; where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules; and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments; exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides; autophagosomes constitutively fuse with MHC class II loading ...

The expression of MHC class II molecules on β-cells of the pancreatic islet has been proposed to play a role in the genesis of insulin-dependent diabetes mellitus in the NOD mouse. We investigated this by immunofluorescent double labeling of islet cells with anti-MHC and anti-CD45 to identify cells of hematopoietic origin. MHC class I expression increased with age on CD45− islet cells. MHC class II expression was not observed on CD45− islet cells at any age; the only cells in the islet that were MHC class II positive were also CD45+. This indicates that all MHC class II-positive cells in the islet are lymphoid cells that infiltrate the islet, whereas the islet endocrine cells express no MHC class II molecules. However, an increase in MHC class I expression occurred on β-cells, and this may play a role in immunopathogenesis.. ...

The ability of the immune system to eliminate and shape the immunogenicity of tumours defines the process of cancer immunoediting1. Immunotherapies such as those that target immune checkpoint molecules can be used to augment immune-mediated elimination of tumours and have resulted in durable responses in patients with cancer that did not respond to previous treatments. However, only a subset of patients benefit from immunotherapy and more knowledge about what is required for successful treatment is needed2-4. Although the role of tumour neoantigen-specific CD8+ T cells in tumour rejection is well established5-9, the roles of other subsets of T cells have received less attention. Here we show that spontaneous and immunotherapy-induced anti-tumour responses require the activity of both tumour-antigen-specific CD8+ and CD4+ T cells, even in tumours that do not express major histocompatibility complex (MHC) class II molecules. In addition, the expression of MHC class II-restricted antigens by tumour cells

MHC Class II (I-A/I-E), PE-eFluor 610, clone: M5/114.15.2, eBioscience™ 25μg; PE-eFluor 610 MHC Class II (I-A/I-E), PE-eFluor 610, clone: M5/114.15.2,...

Anti-MHC Class II antibody conjugated to Biotin [ER-TR3] validated for IHC, Flow Cyt, ICC/IF and tested in Mouse. Referenced in 1 publication. Immunogen…

Helper T cells are stimulated to fight infections or diseases upon recognition of peptides from antigens that are processed and presented by the proteins of Major Histocompatibility Complex (MHC) Class II molecules. Degradation of a full protein into small peptide fragments is a lengthy process consisting of many steps and chaperones. Malfunctions during any step of antigen processing could lead to the development of self-reactive T cells or defective immune response to pathogens. Although much has been accomplished regarding how antigens are processed and presented to T cells, many questions still remain unanswered, preventing the design of therapeutics for direct intervention with antigen processing. Here, we review published work on the discovery and function of a MHC class II molecular chaperone, HLA-DO, in human, and its mouse analog H2-O, herein called DO. While DO was originally discovered decades ago, elucidating its function has proven challenging. DO was discovered in association with

MHC Class II RT1Bu/L antibody [OX-3] (FITC) for FACS. Anti-MHC Class II RT1Bu/L mAb (GTX43381) is tested in Mouse, Rat samples. 100% Ab-Assurance.

HLA class II histocompatibility antigen gamma chain also known as HLA-DR antigens-associated invariant chain or CD74 (Cluster of Differentiation 74), is a protein that in humans is encoded by the CD74 gene. The invariant chain (Abbreviated Ii) is a polypeptide involved in the formation and transport of MHC class II protein. The cell surface form of the invariant chain is known as CD74. The nascent MHC class II protein in the rough ER binds a segment of the invariant chain (Ii; a trimer) in order to shape the peptide binding groove and prevent formation of a closed conformation. Binding to Ii might also prevent binding of peptides from the endogenous pathway to the groove of MHC class II. The invariant chain also facilitates MHC class IIs export from the ER in a vesicle. The signal for endosomal targeting resides in the cytoplasmic tail of the invariant chain. This fuses with a late endosome containing the endocytosed proteins. It is then cleaved by cathepsin S (cathepsin L in cortical thymic ...

We used a hit and run gene targeting strategy to generate mice expressing only the p31 isoform of the conserved invariant (Ii) chain associated with major histocompatibility complex (MHC) class II molecules. Spleen cells from these mice appear indistinguishable from wild type with respect to class II subunit assembly, transport, peptide acquisition, surface expression, and the ability to present intact protein antigens. Moreover, these mutant mice have normal numbers of thymic and peripheral CD4+ T cells, and intact CD4+ T-dependent proliferative responses towards a soluble antigen. In short, MHC class II expression and function are surprisingly unaffected in mice lacking p41 invariant chain, implying that the p31 and p41 isoforms may be functionally redundant in the intact animal.

Accurate prediction of antigen presentation by human leukocyte antigen (HLA) class II molecules would be valuable for vaccine development and cancer immunotherapies. Current computational methods trained on in vitro binding data are limited by insufficient training data and algorithmic constraints. Here we describe MARIA (major histocompatibility complex analysis with recurrent integrated architecture; https://maria.stanford.edu/ ), a multimodal recurrent neural network for predicting the likelihood of antigen presentation from a gene of interest in the context of specific HLA class II alleles. In addition to in vitro binding measurements, MARIA is trained on peptide HLA ligand sequences identified by mass spectrometry, expression levels of antigen genes and protease cleavage signatures. Because it leverages these diverse training data and our improved machine learning framework, MARIA (area under the curve = 0.89-0.92) outperformed existing methods

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HLA class II histocompatibility antigen, DO beta chain is a protein that in humans is encoded by the HLA-DOB gene. HLA-DOB belongs to the HLA class II beta chain paralogues. This class II molecule is a heterodimer consisting of an alpha (DOA) and a beta chain (DOB), both anchored in the membrane. It is located in intracellular vesicles. DO suppresses peptide loading of MHC class II molecules by inhibiting HLA-DM. Class II molecules are expressed in antigen presenting cells (APC: B lymphocytes, dendritic cells, macrophages). The beta chain is approximately 26-28 kDa and its gene contains 6 exons. Exon one encodes the leader peptide, exons 2 and 3 encode the two extracellular domains, exon 4 encodes the transmembrane domain and exon 5 encodes the cytoplasmic tail. ENSG00000241910, ENSG00000243612, ENSG00000239457, ENSG00000241386, ENSG00000241106 GRCh38: Ensembl release 89: ENSG00000243496, ENSG00000241910, ENSG00000243612, ENSG00000239457, ENSG00000241386, ENSG00000241106 - Ensembl, May 2017 ...

Antigen presentation requires intracellular processing of native antigens to produce immunogenic peptides that bind to major histocompatibility complex class II (MHC-II) molecules. In functional studies of antigen processing by elicited peritoneal macrophages, MHC-II-peptide complexes were formed intracellularly. Immunogenic peptides were not released to bind surface MHC-II molecules. Ultrastructural studies employing immunogold staining in ultrathin cryosections of these macrophages showed large amounts of MHC-II molecules in intracellular sac-like vacuoles in the peripheral cytoplasm; most of these were negative for the lamp 1 lysosomal/endosomal membrane protein and cathepsin D. MHC-II molecules were also present in endosomes containing cathepsin D and lamp 1 as well as previously internalized gold-transferrin. The intracellular pool of MHC-II molecules was only slightly decreased by treatment with cycloheximide for 3 hr, indicating that it consisted mainly of endocytosed, recycling molecules, as

Unlike B cells, CD8-positive and CD4-positive T cells of the adaptive immune system do not recognize intact foreign proteins but instead recognize polypeptide fragments of potential antigens. These antigenic peptides are expressed on the surface of antigen presenting cells bound to MHC class I and MHC class II proteins. Here, we review the basics of antigen acquisition by antigen presenting cells, antigen proteolysis into polypeptide fragments, antigenic peptide binding to MHC proteins, and surface display of both MHC class I-peptide and MHC class II-peptide complexes.

Background: The major histocompatibility complex (MHC) is responsible for presenting antigens (epitopes) on the surface of antigen-presenting cells (APCs). When pathogen-derived epitopes are presented by MHC class II on an APC surface, T cells may be able to trigger an specific immune response. Prediction of MHC-II epitopes is particularly challenging because the open binding cleft of the MHC-II molecule allows epitopes to bind beyond the peptide binding groove; therefore, the molecule is capable of accommodating peptides of variable length. Among the methods proposed to predict MHC-II epitopes, artificial neural networks (ANNs) and support vector machines (SVMs) are the most effective methods. We propose a novel classification algorithm to predict MHC-II called sparse representation via 1-minimization. Results: We obtained a collection of experimentally confirmed MHC-II epitopes from the Immune Epitope Database and Analysis Resource (IEDB) and applied our 1-minimization algorithm. To benchmark the

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Sage AP, Nus M, Murphy D, Finigan A, Baker L, Masters L and Mallat Z. Regulatory B cell specific interleukin-10 does not regulate atherosclerosis in mice. ATVB. 35(8):1770-3. doi: 10.1161/ATVBAHA.115.305568. Sage A, Murphy D, Sabir S, Grazia G, Maffia P, Masters L, Baker L, Finigan A, Harrison J, Ludewig B, Reith W, Hansson G, Reizis B, Hugues S, Mallat Z. (2014) MHC class II-restricted antigen presentation by plasmacytoid dendritic cells drives pro-atherogenic immunity. 14;130(16):1363-73. doi: 10.1161/CIRCULATIONAHA.114.011090.. Sage AP & Mallat Z. (2014). Multiple potential roles for B cells in atherosclerosis. Ann Med. doi:10.3109/07853890.2014.900272. Ait-Oufella H, Sage AP, Mallat Z, Tedgui A. (2014). Adaptive (T and B cells) immunity and control by dendritic cells in atherosclerosis. Circ Res, 114(10), 1640-1660. doi:10.1161/CIRCRESAHA.114.302761. Zouggari Y, Ait-Oufella H, Bonnin P, Simon T, Sage A, Guérin C, Vilar J, Caligiuri G, Tsiantoulas D, Laurans L, Dumeau E, Kotti S, Bruneval P, ...

View Rat Monoclonal anti-MHC class II (I-A/I-E) Antibody (M5/114.15.2) [Allophycocyanin] (NBP1-42997). Validated Applications: Flow. Validated Species: Human, Mouse.

The invariant chain (Ii) binds nascent major histocompatibility complex (MHC) class II molecules, blocking peptide binding until the complex dissociates in the endosomes. This may serve to differentiate the MHC class I and II antigen presentation pathways and enable class II molecules to efficiently bind peptides in the endosomes. This hypothesis was addressed by probing spleen cells from a combination of knock-out and transgenic mice with a large panel of T cell hybridomas. The Ii molecule blocked the presentation of a range of endogenously synthesized epitopes, but some epitopes actually required Ii. Thus, the influence of Ii on presentation does not follow simple rules. In addition, mice expressing Ii were not tolerant to epitopes unmasked in its absence, a finding with possible implications for autoimmunity. ...

Males from the BXSB murine strain (H-2b) spontaneously develop an autoimmune syndrome with features of systemic lupus erythematosus (SLE), which results in part from the action of a mutant gene (Yaa) located on the Y chromosome. Like other H-2b mice, the BXSB strain does not express the class II major histocompatibility complex antigen, I-E. Here we report that the expression of I-E (E alpha dE beta b) in BXSB males bearing an E alpha d transgene prevents hypergammaglobulinemia, autoantibody production, and subsequent autoimmune glomerulonephritis. These transgenic mice bear on the majority of their B cells not only I-E molecules, but also an I-E alpha chain-derived peptide presented by a higher number of I-Ab molecules, as recognized by the Y-Ae monoclonal antibody. The I-E+ B cells appear less activated in vivo than the I-E- B cells, a minor population. This limited activation of the I-E+ B cells does not reflect a functional deficiency of this cell population, since it can be stimulated to ...

HLA class II histocompatibility antigen, DQ beta 1 chain; Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for pr ...

Vaccination of colon cancer patients with X-irradiated autologous tumor cells and Bacillus Calmette-Guérin results in a significant reduction in tumor recurrence. A study was undertaken to determine whether the expression of tumor-associated antigens, expression of major histocompatibility complex molecules, or the cellular composition of the vaccine cells correlates with vaccine efficacy. A significant increase in the percentage of histocompatibility leukocyte antigen (HLA) class II molecule-expressing tumor cells was the only marker with a positive correlation. Because HLA class II molecule expression is not a prognostic marker in control patients, it was hypothesized that HLA class II molecules are involved in the induction of tumor immunity in patients treated with the autologous colon tumor vaccine. Enhancement of HLA class II molecule-expressing cells could be induced in X-irradiated colon tumor cells injected into the skin of mice when the cells were mixed with γ-interferon. Therefore, ...

The αβ T-cell coreceptor CD4 enhances immune responses more than 1 million-fold in some assays, and yet the affinity of CD4 for its ligand, peptide-major histocompatibility class II (pMHC II) on antigen-presenting cells, is so weak that it was previously unquantifiable. Here, we report that a soluble form of CD4 failed to bind detectably to pMHC II in surface plasmon resonance-based assays, establishing a new upper limit for the solution affinity at 2.5 mM. However, when presented multivalently on magnetic beads, soluble CD4 bound pMHC II-expressing B cells, confirming that it is active and allowing mapping of the native coreceptor binding site on pMHC II. Whereas binding was undetectable in solution, the affinity of the CD4/pMHC II interaction could be measured in 2D using CD4- and adhesion molecule-functionalized, supported lipid bilayers, yielding a 2D Kd of ∼5,000 molecules/μm(2) This value is two to three orders of magnitude higher than previously measured 2D Kd values for interacting

The structural basis of the interaction between the CD4 coreceptor and a class II major histocompatibility complex (MHC) is described. The crystal structure of a complex containing the human CD4 N-terminal two-domain fragment and the murine I-A(k) class II MHC molecule with associated peptide (pMHCII) shows that only the top corner of the CD4 molecule directly contacts pMHCII. The CD4 Phe-43 side chain extends into a hydrophobic concavity formed by MHC residues from both alpha2 and beta2 domains. A ternary model of the CD4-pMHCII-T-cell receptor (TCR) reveals that the complex appears V-shaped with the membrane-proximal pMHCII at the apex. This configuration excludes a direct TCR-CD4 interaction and suggests how TCR and CD4 signaling is coordinated around the antigenic pMHCII complex. Human CD4 binds to HIV gp120 in a manner strikingly similar to the way in which CD4 interacts with pMHCII. Additional contacts between gp120 and CD4 give the CD4-gp120 complex a greater affinity. Thus, ligation of ...

FUNCTION: Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II ...

Among the parameters controlling the immunodominance of T cell epitopes, it has been proposed that there exists a competition for binding to MHC class II molecules between the processed peptides contained within a single antigenic molecule (14). Experimentally, when mice were immunized with a mixture of two immunogenic peptides of hen egg lysozyme (HEL) having differences in their relative binding capacity to the same class II molecule, the T cell proliferative responses to the weakest binder was inhibited by the strongest binder as a result of MHC occupancy (11). Such in vivo competition between synthetic peptides for binding to MHC was extensively demonstrated (33, 34, 35) and support the hypothesis of peptide competition. However, this hypothesis is based on the artificial situation of immunizations with free peptides, which represent a processed state of the Ag.. In the present study, we tested this hypothesis with bound T cell peptide sequences in a model Ag, MalE. The central question is ...

Infection with L. major is a well-characterized model in which differentiation of class II-restricted T cells into the two mature helper subsets is required for expression of the resistant and susceptible disease phenotype. Ii is required for stable expression of surface class II molecules and, as predicted, cells from Ii −/− mice have substantially lower amounts of surface class II that do not assume the compact conformation that characterizes stable peptide binding ((17), (28), (29)). The major immunologic consequences are twofold: a severely compromised ability to present processed antigens via the class II pathway, and a quantitatively and qualitatively altered CD4+ population due to aberrant selection by thymic epithelial cells unable to present self peptides in a normal manner ((40), (41)). Despite this drastic effect on the class II-dependent immune response, we could discern little consequence to the host in generating either Th1 or Th2 responses to L. major. How might we explain ...

In both collagen-induced arthritis (CIA) and rheumatoid arthritis, T cells recognize a galactosylated peptide from type II collagen (CII). In this study, we demonstrate that the CII259-273 peptide, galactosylated at lysine 264, in complex with Aq molecules prevented development of CIA in mice and ameliorated chronic relapsing disease. In contrast, nonglycosylated CII259-273/Aq complexes had no such effect. CIA dependent on other MHC class II molecules (Ar/Er) was also down-regulated, indicating a bystander vaccination effect. T cells could transfer the amelioration of CIA, showing that the protection is an active process. Thus, a complex between MHC class II molecules and a posttranslationally modified peptide offers a new possibility for treatment of chronically active autoimmune inflammation such as rheumatoid arthritis.

We identified the EphA3 antigen by cotransfecting into 293-EBNA cells a cDNA library from the tumor and cDNA clones coding for CIITA and for the relevant HLA class β II chain. This genetic approach should be generally applicable to clone other genes coding for antigens presented by MHC class II molecules. Although we verified that CIITA induced the expression of Ii in 293-EBNA cells and endowed them with the capacity to present antigens on HLA class II molecules, we observed that the additional cotransfection of an Ii cDNA improved antigen presentation. This proved true for antigens encoded either by the Ii-MAGE-A3 or by the EphA3 cDNA clones (data not shown). A free pool of Ii has been observed in class II-positive cells (31 , 32) , suggesting that an excess of Ii in the endoplasmic reticulum may be important for class II function. This may explain our results.. The name Eph was given to a putative receptor cloned from a human erythropoietin-producing hepatocarcinoma cell line (33 , 34) . Eph ...

The major histocompatibility complex (MHC) is a collection of genes coding for MHC molecules found on the surface of all nucleated cells of the body. In humans, the MHC genes are also referred to as human leukocyte antigen (HLA) genes. Mature red blood cells, which lack a nucleus, are the only cells that do not express MHC molecules on their surface.. There are two classes of MHC molecules involved in adaptive immunity, MHC I and MHC II (Figure 14.11). MHC I molecules are found on all nucleated cells; they present normal self-antigens as well as abnormal or nonself pathogens to the effector T cells involved in cellular immunity. In contrast, MHC II molecules are only found on macrophages, dendritic cells, and B cells; they present abnormal or nonself pathogen antigens for the initial activation of T cells.. Both types of MHC molecules are transmembrane glycoproteins that assemble as dimers in the cytoplasmic membrane of cells, but their structures are quite different. MHC I molecules are ...

While the absence of genes directly encoding MHC class II molecules was similar to the situation in cod [6], the receptor encoding gene (CD8β), which is involved in MHC I recognition via the T-cell receptor (TCR) was absent in pipefish but not cod (table 1). Note that CD8β is not mandatory for a MHC I mediated immune response, as CD8α molecules may function as a homodimer [16]. The antigen recognizing TCR γ was also absent. Because the majority of TCRs consist of α/β-heterodimers, functionality of the TCR is still likely [17].. As opposed to cod, where the CD4+-receptor was truncated and non-functional, this gene could not be identified among pipefish transcripts. For the invariant-chain gene, our annotation returned two contigs that aligned almost perfectly to each other, suggesting the same transcript. When translated into the appropriate amino acid sequence, the putative gene model revealed a stop codon approximately 20 amino acid distant from the 3′-end of the gene in other teleosts ...

IMMUNREAKTION + IMMUNANTWORT (IMMUNOLOGIE); DENDRITISCHE ZELLEN (IMMUNOLOGIE); MHC-KLASSE-II-MOLEKÜLE (IMMUNOLOGIE); ZENTRALNERVENSYSTEM (NEUROLOGIE); IMMUNE REACTION + IMMUNE RESPONSE (IMMUNOLOGY); DENDRITIC CELLS (IMMUNOLOGY); MHC CLASS II MOLECULES (IMMUNOLOGY); CENTRAL NERVOUS SYSTEM (NEUROLOGY ...

MHC II glycoproteins are only present on specialised antigen-presenting cells (APCs), including macrophages that engulf foreign particles such as bacteria, dendritic cells that present antigen to T cells, and B cells that produce antibodies.. ...

Principal nameMHC Class II I-Ak antibodyAlternative names for MHC Class II I-Ak antibodyH2-Aa, H-2 class II histocompatibility antigen A-K alpha…

Antigen presented to CD4+ T cells by major histocompatibility complex class II molecules (MHCII) plays a key role in adaptive immunity. Antigen presentation is initiated by the proteolytic cleavage of pathogenic or self proteins and loading of resultant peptides to MHCII. The loading and exchange of peptides to MHCII is catalyzed by a nonclassical MHCII molecule, HLA-DM (DM). It is well established that DM promotes peptide exchange in vitro and in vivo. However, the mechanism of DM-catalyzed peptide association and dissociation, and how this would affect epitope selection in human responses to infectious disease remain unclear. The work presented in this thesis was directed towards the understanding of mechanism of DM-mediated peptide exchange and its role in epitope selection. In Chapter II, I measured the binding affinity, intrinsic dissociation half-life and DM-mediated dissociation half-life for a large set of peptides derived from vaccinia virus and compared these properties to the peptide-specific

Proximal tubular (PT) epithelial cells express MHC class II (Ia) antigens in immunologically-mediated renal injury. To study the role of PT as accessory cells, we generated several murine PT-like epithelial cell lines by transformation with origin-defective SV40 DNA. These transformed cell lines dis …

The step should be no more than (height of gasket - 1) micrometres to enable flow to be maintained. 44 Lawson, Rose, and Wolf A Glassslide EC monolayer Flow flow chamber B Glass slide flow chamber i ii iii iv Fig. 6. Interposition of a step barrier in the primary flow creates defined areas of disturbed flow downstream. (a) Flow in parallel-plate flow chamber. Laminar flow (black arrows) is created by pumping fluid over an endothelial monolayer plated onto a glass coverslip. (b) Interposition of a step barrier creates areas of disturbed flow downstream: (i) flow recirculation, (ii) flow reattachment, (iii) flow recovery and (iv) recovered laminar shear (adapted from (29)). 1997) Species differences in the expression of major histocompatibility complex class II antigens on coronary artery endothelium: implications for cell-mediated xenoreactivity. Transplantation 64, 1315-22. 4. McDouall RM, Page CS, Hafizi S, Yacoub MH, Rose ML. (1996) Alloproliferation of purified CD4+ T cells to adult human ...

cDCs link innate and adaptive immunity by sensing pathogens and initiating adaptive immune responses. Although the two physiological functions of cDCs are likely to play distinct roles in immune homeostasis, they have not previously been evaluated independently. In the gut, cDCs sense and capture gut microbes in part by extending their processes into the gut lumen (Macpherson and Uhr, 2004; Niess et al., 2005; Chieppa et al., 2006; Vallon-Eberhard et al., 2006). Microbial sensing induces cDCs to produce cytokines such as IL-23, which are required to activate innate lymphoid cells (Kinnebrew et al., 2012; Satpathy et al., 2013). In addition, the ingested microbes are carried to local lymphoid organs, such as the mLNs, processed, and presented to T cells to initiate adaptive immune responses (Macpherson and Uhr, 2004; Niess et al., 2005).. Ablation experiments using CD11cDTR mice, conditional deletion of genes (e.g., Irf4, Irf8, or Notch2) with CD11cCre mice, and Batf3-deficient mice result in ...

TY - JOUR. T1 - Structural Analysis of Invariant Chain Subsets as a Function of Their Association with MHC Class II Chains. AU - Nguyen, Q. V.. AU - Reyes, Victor. AU - Humphreys, R. E.. PY - 1995/2/20. Y1 - 1995/2/20. N2 - Respective subsets of human invariant chain (Ii), as identified with antibodies to two different epitopes, were characterized as a function of their associations with major histocompatibility complex (MHC) class II α,β chains and intracellular processing. E1 antiserum to Ii(183-193) and VIC-Y1 monoclonal antibody to an N-terminal determinant identified Ii(E1) and Ii(VIC) populations, respectively. Ii proteins comprise several species which have been defined with either genomic or post-translational processes: Ii itself; IpN and IpO, which represent the glycosylated forms on asparagine or threonine/serine, respectively; γ2 and γ3, which originate from an alternative initiation site for transcription; and p41, which has a 64-amino-acid insert which originated from an ...

2oje: Zinc induces dimerization of the class II major histocompatibility complex molecule that leads to cooperative binding to a superantigen.

Looking for online definition of major histocompatability complex in the Medical Dictionary? major histocompatability complex explanation free. What is major histocompatability complex? Meaning of major histocompatability complex medical term. What does major histocompatability complex mean?

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One of the long term goals of our research is to determine why the maternal immune system does not reject the genetically disparate fetus during pregnancy. Our studies are focused primarily on the immunoregulatory properties of trophoblast cells, which are the first cells to differentiate from the embryo, and ultimately form the fetal component of the placenta. Trophoblast cells are the only cells derived from the blastocyst that are in direct contact with maternal blood, and therefore play an essential role in protecting the fetus from attack from the maternal immune system. Trophoblast cells are relatively unique in that they do not express major histocompatibility complex (MHC) class II antigens, either constitutively, or after exposure to IFN-gamma. The absence of MHC class II antigen expression on trophoblast cells is thought to be critical for prevention of deleterious maternal immune responses against the fetus. Thus, successful reproduction of mammals may require that MHC class II gene ...

The antigen-presenting abilities of basophils and their role in initiating a Th2 phenotype is a topic of current controversy. We aimed to determine whether human basophils can be induced to express MHC Class II and act as antigen presenting cells for T cell stimulation. Isolated human basophils were exposed to a panel of cytokines and TLR-ligands and assessed for MHC Class II expression. MHC Class II was expressed in up to 17% of isolated basophils following incubation with a combination of IL-3, IFN-γ and GM-CSF for 72 hours. Costimulatory molecules (CD80 and CD86) were expressed at very low levels after stimulation. Gene expression analysis of MHC Class II-positive basophils confirmed up-regulation of HLA-DR, HLA-DM, CD74 and Cathepsin S. However, MHC Class II expressing basophils were incapable of inducing antigen-specific T cell activation or proliferation. This is the first report of significant cytokine-induced MHC Class II up-regulation, at both RNA and protein level, in isolated human ...

Proteolysis of the class II-associated invariant chain generates a peptide binding site in intracellular HLA-DR molecules. Proc. Natl. Acad. Sci. USA. 1991. 88:

TY - JOUR. T1 - Analysis of T-cell hybridomas with an unusual MHC class II-dependent ligand specificity. AU - Mendiratta, S. K.. AU - Singh, Nagendra. AU - Bal, V.. AU - Rath, S.. PY - 1996/1/1. Y1 - 1996/1/1. N2 - We have characterized two unusual T-cell hybridomas, 1E3 and 3B8, from H-2(k) mice immunized with I-Ab-transfected L cells (H-2(k)), that are stimulated by L cells transfected with I-Ab, I-A(k) or I-Eb, but not by non-transfected L cells. These hybridomas could not be stimulated by spleen cells from H-2(i3), H-2(k), H-2b or H-2(d) mice. Monoclonal anti-I-A antibodies did not block their responses, suggesting that mouse major histocompatibility complex (MHC) class II molecules may be peptide donors rather than restriction elements for them. The stimulation of these hybridomas by fibroblast targets was not blocked by an anti-H-2k(k),D(k)-specific monoclonal antibody. Lipopolysaccharide (LPS)-activated splenic and peritoneal exudate cells from H-2(k), H-2(d), H-2(i3), H-2b as well as ...

RefSeq Summary (NM_002118): HLA-DMB belongs to the HLA class II beta chain paralogues. This class II molecule is a heterodimer consisting of an alpha (DMA) and a beta (DMB) chain, both anchored in the membrane. It is located in intracellular vesicles. DM plays a central role in the peptide loading of MHC class II molecules by helping to release the CLIP (class II-associated invariant chain peptide) molecule from the peptide binding site. Class II molecules are expressed in antigen presenting cells (APC: B lymphocytes, dendritic cells, macrophages). The beta chain is approximately 26-28 kDa and its gene contains 6 exons. Exon one encodes the leader peptide, exons 2 and 3 encode the two extracellular domains, exon 4 encodes the transmembrane domain and exon 5 encodes the cytoplasmic tail. [provided by RefSeq, Jul 2008]. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Gene record to access additional publications. ...

TY - JOUR. T1 - Cathepsin S activity is detectable in human keratinocytes and is selectively upregulated upon stimulation with interferon-gamma. AU - Schwarz, Gerold. AU - Boehncke, Wolf-Henning. AU - Braun, Manuela. AU - Schröter, Christian J. AU - Burster, Timo. AU - Flad, Thomas. AU - Dressel, Daniela. AU - Weber, Ekkehard. AU - Schmid, Heide. AU - Kalbacher, Hubert. PY - 2002/7. Y1 - 2002/7. N2 - Keratinocytes are an integral component of the skin immune system and function as nonprofessional antigen-presenting cells in pathophysiologic conditions when they express major histocompatibility complex class II molecules, e.g., in psoriasis. In order to analyze further this function we investigated the activity of cathepsin S in comparison with cathepsins B and L. These enzymes were suggested to be involved in antigen presentation. Specific catalytic activities of these cathepsins were determined fluorometrically by hydrolysis of a synthetic substrate (Z-Phe-Arg-7-amido-4-methylcoumarin) in ...

Type 1 Diabetes is an autoimmune condition in which segments of the immune system cause the destruction of insulin producing cells in the pancreas, leaving individuals with an impaired ability to control blood glucose levels. Currently there is no cure for Type 1 Diabetes and the treatments involve lifelong insulin administration and careful monitoring of blood glucose levels. Long-term complications like cardiovascular disease, nerve damage, and retina damage, may result. Previous studies have shown that improvement in the control of blood glucose can reduce the risks from these long-term complications. Residual insulin production, typically within the first few years following diagnosis, helps to reduce an individuals need to supplement insulin by injection or pump. This effect helps in maintaining the bodys ability to regulate blood glucose levels and reducing the needs of external insulin.. Methyldopa, or Aldomet, has been approved by the Food and Drug Administration and is commonly used ...

HLA Class II molecules are expressed by human thyroid epithelial cells (thyrocytes) in thyroid autoimmunity, although these cells are normally Class II-. gamma-Interferon (gamma-IFN) is probably involved in this expression, as suggested by its ability to induce Class II in cultured normal thyrocytes. We have now found that thyroid stimulating hormone (TSH) enhances Class II expression induced in cultured thyrocytes by gamma-IFN, and effects similar to those of TSH were obtained with dibutyryl cyclic AMP. A proportion of thyrocytes also expressed Class II following treatment with TSH or dibutyryl cyclic AMP in the absence of gamma-IFN, but the optimal activity of these mediators then appeared to be dependent upon the occurrence of some pre-existing Class II expression. These findings give insights into how a variety of mediators may influence Class II expression in thyroid autoimmunity.

Yilla, M.; Hickman, C.; McGrew, M.; Meade, E.; Bellini, W.J., 2003: Edmonston measles virus prevents increased cell surface expression of peptide-loaded major histocompatibility complex class II proteins in human peripheral monocytes

AE37 peptide/GM-CSF vaccine: A vaccine containing HER2/Neu-derived epitope (amino acids 776-790) linked to li-Key peptide (li-Key/HER2/neu hybrid peptide or AE37), and combined with granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential antineoplastic and immunoadjuvant activities. Upon vaccination, AE37 may activate the immune system and stimulate T-helper cells against HER2/Neu expressing cancer cells. GM-CSF may potentiate the immune response against cancer cells expressing the HER2/Neu antigen. The Ii-Key moiety, a 4-amino acid (LRMK) epitope from the MHC class II-associated invariant chain (Ii protein), increases T-helper cell stimulation against HER2/neu antigen when compared to unmodified class II epitopes. HER2/neu, a tumor associated antigen (TAA), is overexpressed in a variety of tumor cell types and is highly immunogenic. Check for active clinical trials or closed clinical trials using this agent. (NCI Thesaurus) -- from cancer.gov ...

Neutrophil Activation of Endothelial Cell-Expressed TRPM2 Mediates Transendothelial Neutrophil Migration and Vascular Injury Investigators addressed the possible role of transient receptor potential melastatin-2 (TRPM2) expressed in endothelial cells (ECs) in the mechanism of transendothelial migration of polymorphonuclear leukocytes (PMNs). They observed defective PMN transmigration in response to LPS challenge in adult mice in which the EC expressed TRPM2 was conditionally deleted. [Circ Res] Abstract Ex Vivo Pretreatment of Human Vessels with siRNA Nanoparticles Provides Protein Silencing in Endothelial Cells The authors report the development of small interfering RNA-releasing poly(amine-co-ester) nanoparticles, distinguished by their high content of a hydrophobic lactone. They showed that a single transfection of small interfering RNA targeting class II transactivator attenuates major histocompatibility complex class II expression on endothelial cells for at least four to six weeks after ...

MHC class II presentation of antigenic peptides derived from soluble proteins is usually preceded by antigenic uptake via (nonreceptor-mediated) endocytosis by professional APCs, followed by processing in endosomal compartments. Although in vitro alternative pathways for MHC class II loading have been described for certain intracellularly synthesized proteins, the importance of these pathways has not been assessed in vivo. We have shown previously that endogenously produced membrane-associated glycoprotein (GP) of lymphocytic choriomeningitis virus (LCMV), a noncytopathic virus, can be presented in vitro on MHC class II molecules in the absence of the invariant chain (Ii), whereas the cytosolic LCMV nucleoprotein (LCMV-NP) failed to be presented under the same conditions. Taking advantage of this system, we analyzed presentation of LCMV-GP and LCMV-NP in vivo in Ii-deficient mice and followed the induced Th cell and B cell responses. At early time points after LCMV infection of li-deficient mice, we

Major histocompatibility (MHC) class II molecules are strongly associated with many autoimmune disorders. In type 1 diabetes, the DQ8 molecule is common, confers significant disease risk and is involved in disease pathogenesis. We hypothesized blocking DQ8 antigen presentation would provide therapeutic benefit by preventing recognition of self-peptides by pathogenic T cells. We used the crystal structure of DQ8 to select drug-like small molecules predicted to bind structural pockets in the MHC antigen-binding cleft. A limited number of the predicted compounds inhibited DQ8 antigen presentation in vitro with one compound preventing insulin autoantibody production and delaying diabetes onset in an animal model of spontaneous autoimmune diabetes. An existing drug of similar structure, methyldopa, specifically blocked DQ8 in recent-onset patients with type 1 diabetes along with reducing inflammatory T cell responses toward insulin, highlighting the relevance of blocking disease-specific MHC class II ...

Major histocompatibility (MHC) class II molecules are strongly associated with many autoimmune disorders. In type 1 diabetes, the DQ8 molecule is common, confers significant disease risk and is involved in disease pathogenesis. We hypothesized blocking DQ8 antigen presentation would provide therapeutic benefit by preventing recognition of self-peptides by pathogenic T cells. We used the crystal structure of DQ8 to select drug-like small molecules predicted to bind structural pockets in the MHC antigen-binding cleft. A limited number of the predicted compounds inhibited DQ8 antigen presentation in vitro with one compound preventing insulin autoantibody production and delaying diabetes onset in an animal model of spontaneous autoimmune diabetes. An existing drug of similar structure, methyldopa, specifically blocked DQ8 in recent-onset patients with type 1 diabetes along with reducing inflammatory T cell responses toward insulin, highlighting the relevance of blocking disease-specific MHC class II ...

Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.

Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.

TY - JOUR. T1 - A murine retrovirus induces proliferation of unique lymphoid cell lines expressing T-cell-receptor structures utilizing common variable region alpha and beta chain genes. AU - ONeill, H C. PY - 1993/4/1. Y1 - 1993/4/1. N2 - A murine radiation leukemia virus (RadLV) has been shown to induce in vitro proliferation of an unusual subset of lymphoid cells from spleen. They have the unusual property of expressing CD3/T-cell receptor alpha and beta chains (TCR-alpha beta) in the absence of other T-cell markers such as Thy-1, CD4, and CD8. Cell lines induced in two mouse strains with RadLV produced by the C6VL/1 thymoma all specifically utilize common V alpha 3 and V beta 8.2 variable region genes in the formation of a TCR structure. Each of these cell lines has now been found to express both class I and class II major histocompatibility antigens and the beta 2 integrin specific for spleen dendritic cells. Analysis of functional properties of these cells has revealed a subset that can ...

Human atheromata, but not normal blood vessels, contain numerous smooth muscle cells (SMC) that bear class II major histocompatibility (MHC) antigens. These lesions also contain leukocytes that can secrete cytokines, which may modulate SMC functions. Because of morphologic evidence for immune-activated (class II+) SMC in vascular lesions, we studied the regulation by cytokines of MHC gene expression in SMC cultured from human vessels. Under basal conditions, these SMC contained mRNA for class I MHC (detected by Northern blotting with a cDNA probe for HLA-B7) and expressed surface class I MHC product determined by enzyme-linked immunoassay with monoclonal antibody (MAb) W6/32. Unstimulated SMC contained little or no class II MHC mRNA (probed with HLA-DR alpha cDNA) or surface antigen (examined using MAb I2). Secretory products of activated human leukocytes (the cell-free supernatant of a mixed leukocyte reaction) induced class II MHC antigen expression by SMC after 3 days. Treatment of SMC with ...

HLA class II expression is notable in rheumatoid arthritis. We have investigated the mechanism of HLA class II regulation in the joints and found local synthesis, as judged by mRNA levels to be high. The role of antigen presentation in maintaining class II mRNA was explored, and blocking presentation by using monoclonal antibodies to HLA class II inhibited synthesis of mRNA for HLA-DR alpha chain. HLA class II expression is maintained by cytokines and so cytokine production in rheumatoid joints was investigated. It was chosen to use mRNA analysis by slot blotting as a screening assay, and the expression of many cytokines was detected. Levels of these were maintained in culture in the absence of extrinsic stimulation.

We have examined the ability of hCD4 to interact functionally with mouse class II MHC molecules using the mouse T cell hybridoma BI-141, specific for beef insulin. We have previously shown that expression of mouse CD4 results in a marked enhancement of IL-2 release by BI-141 cells in response to beef insulin or, in a cross-reactive response, to pork insulin, on the appropriate mouse APCs. We now demonstrate that expression of hCD4 results in an equivalent stimulation of antigen responses by this mouse T cell hybridoma. The specificity of this effect was demonstrated by mAb and gp120 blocking studies. These data provide the first direct evidence for function of hCD4 and in an exclusively mouse system. ...

Hello, thank you for visiting my blog. I am Tankeshwar Acharya. Blogging is my passion. I am working as an Asst. Professor and Microbiologist at Department of Microbiology and Immunology, Patan Academy of Health Sciences, Nepal. If you want me to write about any posts that you found confusing/difficult, please mention in the comments below ...

Antigen presentation to T lymphocytes has been characterized extensively in terms of T lymphocyte activation and eventual cell death. In contrast, little is known about the consequences of antigen presentation for the antigen-presenting cell (APC). We have determined the outcome of major histocompatibility complex class II-restricted peptide presentation to a specific T cell. We demonstrate that specific T lymphocyte interaction with peptide-presenting APCs led to apoptosis in the APC population. In contrast, T lymphocyte interaction with nonpeptide-loaded APCs or APCs loaded with monosubstituted peptide failed to induce T lymphocyte secretion of interleukin-2 and APC apoptosis. Phosphatidylserine externalization and mitochondrial depolarization were used to evaluate APC apoptosis. Fas/Fas ligand interactions were not required, but cytoskeletal integrity and caspase activation were essential for APC apoptosis. Antigen presentation leading to T lymphocyte activation is therefore coordinated with

Over the last decade, our understanding and ability to predict the MHC class I pathway antigen presentation has improved substantially. This however does not hold for post-transnationally modified (PTM) antigens, where our understanding on how PTMs impact the potential for antigen presentation remains limited. Likewise, is our ability to predict MHC class II antigen presentation limited, and data suggest that properties other that MHC binding plays a critical role for the prediction of CD4 epitopes. Finally, is our understanding of the role of the T cell and the similarity of the presented peptide to the self proteome in the context of peptide immunogenicity very limited ...

DNA vaccines promote an immune response by providing antigen-encoding DNA to the recipient, but the efficacy of such vaccines needs improving. Many approaches have considerable potential but currently induce relatively weak immune responses despite multiple high doses of DNA vaccine. Here, we asked whether targeting vaccine antigens to DCs would increase the immunity and protection that result from DNA vaccines. To determine this, we generated a DNA vaccine encoding a fusion protein comprised of the vaccine antigen and a single-chain Fv antibody (scFv) specific for the DC-restricted antigen-uptake receptor DEC205. Following vaccination of mice, the vaccine antigen was expressed selectively by DCs, which were required for the increased efficacy of MHC class I and MHC class II antigen presentation relative to a control scFv DNA vaccine. In addition, a DNA vaccine encoding an HIV gag p41-scFv DEC205 fusion protein induced 10-fold higher antibody levels and increased numbers of IFN-γ-producing CD4+ ...

HIV-specific CD4+ T helper lymphocytes are preferred targets for infection. Although complete interruption of combination antiretroviral therapy (ART) can form part of therapeutic manipulations, there is grave concern that the resumption of viral replication might destroy, perhaps irreversibly, these T helper populations. High viremia blocks the proliferation capacity of HIV-specific helper cells. However, cytokine production assays imply that some antigen-specific effector function is retained. Despite this careful work, it remains unclear whether the return of HIV-1 replication physically destroys HIV-1-specific T helper cells in the peripheral blood. Difficulties in producing stable peptide-MHC class II complexes and the very low frequencies of antigen-specific CD4+ T cells have delayed the application of this powerful technique. Here we employ HLA class II tetramers and validate a sensitive, quantitative cell-enrichment technique to detect HIV-1 T helper cells. We studied patients with early-stage

MHC-II antigen presentation by W cells is usually important in order for W cells to receive ideal costimulation from helper Compact disc4+ T cells. blend partner was created in the 1970s to generate B-cell hybridomas that secrete monoclonal antibodies (Kohler and Milstein, 1975). Thereafter Shortly, this technique was used to Capital t cells to create T-cell hybridomas that secrete IL-2 after TCR signaling (Kappler et al., 1982; Rock and roll et al., 1990). In light of the useful advantages of using peptide-specific T-cell hybridomas, researchers possess broadly used them as a device to quantitatively measure peptide-specific antigen demonstration by multiple types of antigen showing cells (APC). Vidovic et al exhibited that the adhesion substances and integrins in human being and murine Capital t cells are extremely extremely functionally conserved and murine T-cell:human being APC conversation happened easily (Vidovic et al., 2003). We and others possess utilized HLA-DR transgenic rodents to ...

MO-DC generated in vitro serve as a model type of DC to unravel the complex interactions among DC maturation, MHC class II peptide loading, and endocytic transport (3, 33, 34). The emerging picture suggests that endocytic protease activity is regulated by differential activity of the lysosomal ATPase during DC maturation (3). By analyzing lysosomal MBP processing at pH 5.0 in vitro, we have here mimicked the conditions present in the lysosomal compartment of DC in the activated state in vivo.. The MHC class II-associated proteolytic machinery is characterized by a hierarchical proteolytic cascade, where the initial step controls the efficiency of Ag processing, peptide presentation, and T cell activation (14). Different types of APC as well as primary cells and immortalized cell lines contain distinct activity patterns of endocytic proteases (11, 17, 31, 35, 36, 37) which might result in different processing pathways for a given Ag and hence in different selections of peptides presented. We here ...

Improved risk models of patients with stage III melanoma will improve the treatment of patients with this disease; however, molecular markers are lacking. Our analysis of independent cohorts (two for protein in TMA, and one for mRNA in TCGA) of patients tumors strongly implicates increased CD74 expression as a new marker of good prognosis in stage III melanoma. Previously, we had considered inflammatory markers to be associated with poor prognosis, which was the case for MIF in both cohorts, and for iNOS in the MDACC cohort. The surprising finding of higher expression of CD74 having a strong association with good prognosis is most intriguing, and elucidating the mechanism involved is likely to open new avenues for melanoma research.. The functional role of CD74 is not well understood. Historically, CD74 was known primarily as the MHC class II invariant chain and functions in the molecular processing of MHC II through the Golgi (24). It has a potential role in the antitumor immune response (25), ...

As a severe chronic metabolic disease and autoimmune disorder, type 1 diabetes (T1D) affects millions of people world-wide. Recent advances in antigen-based immunotherapy have provided a great opportunity for further treating T1D with a high degree of selectivity. It is reported that MHC class II I-Ag7 in the non-obese diabetic (NOD) mouse and human HLA-DQ8 are strongly linked to susceptibility to T1D. Thus, the identification of new I-Ag7 and HLA-DQ8 epitopes would be of great help to further experimental and biomedical manipulation efforts. In this study, a novel GPS-MBA (MHC Binding Analyzer) software package was developed for the prediction of I-Ag7 and HLA-DQ8 epitopes. Using experimentally identified epitopes as the training data sets, a previously developed GPS (Group-based Prediction System) algorithm was adopted and improved. By extensive evaluation and comparison, the GPS-MBA performance was found to be much better than other tools of this type. With this powerful tool, we predicted a number

T-cell receptor MHC complex. Computer model showing the structure of a T-cell surface glycoprotein CD4 (purple) complexed to the H-2 class II histocompatibility antigen A-K alpha chain (green) beta chain (yellow) and ovotransferrin (red). CD4 is a receptor found on T-cell white blood cells of the immune system. Antigens (foreign proteins) are presented to T cell receptors by MHC molecules to effect an immune response. - Stock Image C035/5403

J Immunol. 2001 Oct 1;167(7):3626-34. Harton JA, Zika E, Ting JP. The histone acetyltransferase domains of CREB-binding protein (CBP) and p300/CBP-associated factor are not necessary for cooperativity with the class II transactivator. J Biol Chem. 2001 Oct 19;276(42):38715-20. Deffrennes V, Vedrenne J, Stolzenberg MC, Piskurich J, Barbieri G, Ting JP, Charron D, Alcaide-Loridan C. Constitutive expression of MHC class II genes in melanoma cell lines results from the transcription of class II transactivator abnormally initiated from its B cell-specific promoter. J Immunol. 2001 Jul 1;167(1):98-106. Li G, Harton JA, Zhu X, Ting JP. Downregulation of CIITA function by protein kinase a (PKA)-mediated phosphorylation: mechanism of prostaglandin E, cyclic AMP, and PKA inhibition of class II major histocompatibility complex expression in monocytic lines. Mol Cell Biol. 2001 Jul;21(14):4626-35. Linhoff MW, Harton JA, Cressman DE, Martin BK, Ting JP. Two distinct domains within CIITA mediate ...

Recent gene expression studies have suggested that down-regulation of HLA class II expression has a major biological effect reflected in clinical tumor characteristics and outcome. This has been shown for B-cell lymphomas, that naturally express HLA class II on lymphoma cells (8, 22), but also for carcinomas in which HLA class II can be expressed on the antigen-presenting cells within the tumor (24). It is increasingly appreciated that not only HLA class I but also class II is essential for mounting an adequate antitumor immune response. Antigen presentation via HLA class II is indispensable to activate a CD4+ T-cell population that may induce a CD8+ T cell-mediated cytotoxic antitumor response (25, 26) and recruit additional effector cell populations, such as macrophages (26, 27). In carcinomas, an immune-mediated antitumor response is mainly mediated by professional antigen-presenting cells.. In B-cell lymphomas, both professional antigen-presenting cells as well as the tumor B cells may play ...

Link to Pubmed [PMID] - 14517277. J. Exp. Med. 2003 Oct;198(7):1089-102. The exact role of major histocompatibility complex (MHC) molecules in the peripheral survival of naive T cells is controversial, as some studies have suggested that they are critically required whereas others have suggested that they are not. Here we controlled for some of the features that differed among the earlier studies, and analyzed both the survival and expansion of naive CD4+ T cells transferred into MHC syngeneic, allogeneic, or MHC negative environments. We found that naive T cells transferred into MHC negative or allogeneic environments often fail to survive because of rejection and/or competition by natural killer (NK) cells, rather than failure to recognize a particular MHC allele. In the absence of NK cells, naive CD4+ T cells survived equally well regardless of the MHC type of the host. There was, however, an MHC requirement for extensive space-induced homeostatic expansion. Although the first few divisions ...

TY - JOUR. T1 - Apoptotic DNA binds to HLA class II molecules inhibiting antigen presentation and participating in the development of anti-inflammatory functional behavior of phagocytic macrophages. AU - Filaci, Gilberto. AU - Contini, Paola. AU - Fravega, Marco. AU - Fenoglio, Daniela. AU - Azzarone, Bruno. AU - Julien-Giron, Michel. AU - Fiocca, Roberto. AU - Boggio, Maurizio. AU - Necchi, Vittorio. AU - De Lerma Barbaro, Andrea. AU - Merlo, Andrea. AU - Rizzi, Marta. AU - Ghio, Massimo. AU - Setti, Maurizio. AU - Puppo, Francesco. AU - Zanetti, Maurizio. AU - Indiveri, Francesco. PY - 2003/1/1. Y1 - 2003/1/1. N2 - Resident macrophages are mainly responsible for the clearance of apoptotic cells from tissue by phagocytosis. Phagocytosis of apoptotic cells is not accompanied by activation of inflammatory mechanisms, unlike what happens when necrotic phenomena occur. We analyzed the effect of phagocytosis of apoptotic bodies on macrophage cell functions. After phagocytosis of apoptotic cells ...

Major Histocompatibility Complex (MHC) glycoproteins are heterodimeric cell surface receptors that function to present antigen peptide fragments to T cells responsible for cell-mediated immune responses. MHC molecules can be subdivided into two groups on the basis of structure and function: class I molecules present intracellular antigen peptide fragments (~10 amino acids) on the surface of the host cells to cytotoxic T cells; class II molecules present exogenously derived antigenic peptides (~15 amino acids) to helper T cells. MHC class I and II molecules are assembled and loaded with their peptide ligands via different mechanisms. However, both present peptide fragments rather than entire proteins to T cells, and are required to mount an immune response.. Class II MHC glycoproteins are expressed on the surface of antigen-presenting cells (APC), including macrophages, dendritic cells and B cells. MHC II proteins present peptide antigens that originate extracellularly from foreign bodies such as ...

MHC Class II I-Ab Mouse anti-Mouse, PE, Clone: AF6-120.1, eBioscience™ 100μg; PE MHC Class II I-Ab Mouse anti-Mouse, PE, Clone: AF6-120.1, eBioscience™...

Animals; Antigens, CD/metabolism; Antigens, CD5/metabolism; Antigens, Differentiation, T-Lymphocyte/metabolism; CD4-Positive T-Lymphocytes/cytology; CD4-Positive T-Lymphocytes/immunology; CD8-Positive T-Lymphocytes/cytology; CD8-Positive T-Lymphocytes/immunology; Cell Differentiation; DNA-Binding Proteins/metabolism; Flow Cytometry; Gene Expression Regulation; Histocompatibility Antigens Class I/immunology; Histocompatibility Antigens Class I/metabolism; Histocompatibility Antigens Class II/immunology; Histocompatibility Antigens Class II/metabolism; Humans; Jurkat Cells; Lectins, C-Type; Liver/cytology; Liver/embryology; Membrane Proteins/genetics; Membrane Proteins/metabolism; Mice; Mice, Transgenic; NFATC Transcription Factors; Nuclear Proteins; Promoter Regions, Genetic/genetics; Receptor, Notch1; Receptors, Antigen, T-Cell/genetics; Receptors, Antigen, T-Cell/immunology; Receptors, Antigen, T-Cell/metabolism; Receptors, Cell Surface; Response Elements/genetics; Signal Transduction; Thymus ...

The OKT4 antibody reacts with human CD4, a 59 kDa protein which acts as a co-receptor for the T cell receptor (TCR) in its interaction with MHC Class II molecules on antigen-presenting cells. The extracellular domain of CD4 binds to the beta-2 domain of MHC Class II, while its cytoplasmic tail provides a binding site f