Antigenic Modulation
Antigen-Antibody Reactions
Myasthenia Gravis
Antigens, Surface
Antigen-Antibody Complex
Establishment of a human thymic myoid cell line. Phenotypic and functional characteristics. (1/22)
The subset of myoid cells is a normal component of the thymic stroma. To characterize these cells, we immortalized stromal cells from human thymus by using a plasmid vector encoding the SV40 T oncogene. Among the eight cell lines obtained, one had myoid characteristics including desmin and troponin antigens. This new line was designated MITC (myoid immortalized thymic cells). These cells expressed both the fetal and adult forms of muscle acetylcholine receptor (AChR) at the mRNA level, as well as the myogenic transcription factor MyoD1. alpha-Subunit AChR protein expression was detected by flow cytometry and the AChR was functional in patch-clamp studies. In addition, AChR expression was down-modulated by myasthenia gravis sera or by monoclonal antibody anti-AChR on MITC line similarly to TE671 rhabdomyosarcoma cells, making the MITC line an interesting tool for AChR antigenic modulation experiments. Finally, the MITC line expressed LFA-3, produced several cytokines able to act on T cells, and protected total thymocytes from spontaneous apoptosis in vitro. These results are compatible with a role of thymic myoid cells in some steps of thymocyte development. Therefore MITC line appears to be a useful tool to investigate the physiological role of thymic myoid cells. (+info)Nematode infection enhances survival of activated T cells by modulating accessory cell function. (2/22)
The type of immune response generated following exposure to Ag depends on a variety of factors, including the nature of the Ag, the type of adjuvant used, the site of antigenic entry, and the immune status of the host. We have previously shown that infection of rodents with Nippostrongylus brasiliensis (Nb) shifts the development of type 1 allo-specific responses toward type 2 immunity, suggesting nematode modulation of T cell activation. In this report we explore the immunomodulatory effects of Nb on T cell activation. We found that spleen cells from Nb-infected mice exhibited dramatically increased proliferation in response to Con A and anti-CD3. This hyperproliferation could be transferred in vitro to naive splenocytes by coculture with mitomycin C-treated cells from Nb-infected animals. The transfer was mediated by non-T accessory cells and supernatants derived from Con A-activated non-T cells, suggesting the involvement of a soluble factor secreted by accessory cells. The accessory cells secreted high levels of IL-6, and anti-IL-6 treatment abrogated the supernatant-induced hyperproliferation, thus confirming that IL-6 was mediating the effect. Further, spleen cells from Nb-infected mice were more resistant to activation-induced cell death (AICD) following mitogenic stimulation. Reduced AICD was also transferable and IL-6 dependent. Thus, the hyperproliferation was in part due to enhanced activated T cell survival. These phenomena mediated by accessory cells may contribute to the powerful polyclonal activation of type 2 immunity caused by nematode infection. (+info)Modulation of multiple experimental arthritis models by collagen-induced arthritis quantitative trait loci isolated in congenic rat lines: different effects of non-major histocompatibility complex quantitative trait loci in males and females. (3/22)
OBJECTIVE: Collagen-induced arthritis (CIA) is a model of inflammatory arthritis with many similarities to rheumatoid arthritis (RA). We previously mapped in F(2) offspring of CIA-susceptible DA and CIA-resistant F344 rats, 5 quantitative trait loci (QTLs) for which F344 alleles were associated with reduced CIA severity. In the present study, we sought to characterize the independent arthritis-modulating effects of these 5 QTLs. METHODS: CIA-regulatory regions were transferred from the F344 genome to the DA background or vice versa by repeated backcrossing. The arthritis-modulating effects of the transferred alleles were determined by comparing the severity of experimentally induced arthritis in congenic rats with that in DA rats. RESULTS: Congenic lines with either the F344 major histocompatibility complex (MHC) on the DA background or the DA MHC on the F344 background were resistant to CIA, confirming both MHC and non-MHC contributions to the genetic regulation of CIA. F344 alleles at the Cia3 and Cia5 regions of chromosomes 4 and 10 reduced CIA severity relative to that observed in DA rats. F344 Cia4 and Cia6 regions of chromosomes 7 and 8 failed to significantly alter CIA severity. Arthritis-modifying effects of Cia4 and Cia6 were, however, detected in pristane-induced and/or Freund's incomplete adjuvant oil-induced arthritis. The arthritis-modifying effects of the non-MHC CIA-regulatory loci differed in males and females. CONCLUSION: These congenic lines confirmed the existence and location of genes that regulate the severity of experimental arthritis in rats. Mechanisms responsible for the sex-specificity of individual arthritis-regulatory loci may explain some of the sex differences observed in RA and other autoimmune diseases in humans. (+info)Cell membrane modification for rapid display of proteins as a novel means of immunomodulation: FasL-decorated cells prevent islet graft rejection. (4/22)
Long-term display of exogenous proteins on the cell surface may have important research and therapeutic implications. We report a novel method for the cell-surface display of proteins that involves generation of a chimeric protein with core streptavidin, biotinylation of cells, and "decoration" with the protein. A chimeric protein with the extracellular portions of FasL (SA-FasL) was efficiently displayed on the cell surface within 2 hr without detectable cellular toxicity. Biotin and SA-FasL persisted on the cell surface for weeks in vitro and in vivo. Immunomodulation with SA-FasL-decorated splenocytes effectively blocked alloreactive responses in naive and presensitized rodents and prevented the rejection of allogeneic pancreatic islets. This approach may serve as an alternative to gene transfer-based expression with broad research and therapeutic applications. (+info)T-cell subset analysis of Lewis lung carcinoma tumor rejection: heterogeneity of effectors and evidence for negative regulatory lymphocytes correlating with metastasis. (5/22)
We have analyzed the phenotypes of the T-cell subsets generated in response to Lewis lung carcinoma clones in C57BL/6J recipients. The metastatic derivative, which expresses low levels of H-2Kb gene, predominantly elicited CD8, V beta 8, and V beta 9+ T-cells. The nonmetastatic clone expressing high levels of H-Kb gene triggered a more heterogeneous response of V beta-5, -6, -8, -9, and -11 CD8+ T-cells. Comparison of the T-cell receptor (TCR) expression of the T-cells infiltrating the tumor site with the lymphocytes in the periphery of tumor-bearing animals revealed a pattern of homing of CD4+ T-cells bearing V beta-5, -6, and -11 TCR chains and CD8+ T-cells bearing V beta-5, -6, -9, and -11. Depletion of V beta 5 or V beta 6+ T-cells correlated with accelerated tumor growth, implying their protective role as tumor-specific effectors and consistent with the cytotoxicity of T-cells with this TCR phenotype. V beta 11 TCR expression in the tumor-infiltrating lymphocytes increased with the tumor size. Depletion of V beta 11+ T-cells enhanced resistance to primary tumor growth and conferred protection from metastasis in recipients cleared of V beta 5 and V beta 6 T-cell subsets. Those results suggest that tumor-specific effectors as well as negative regulator T-cells home, infiltrate, and coexist in the tumor site. (+info)Expression of major histocompatibility complex class II and costimulatory molecules in oral carcinomas in vitro. (6/22)
Recognition in the 1980 s that keratinocytes can express class II molecules of the Major Histocompatibility Complex (MHC) first raised the possibility that these cells might have an immunological function, and may even act as antigen presenting cells (APC). For effective T lymphocyte activation, APC require, in addition to MHC II, appropriate costimulatory signals. The aim of this study was to determine the expression of MHC class II and the co-stimulatory molecules CD40, CD80 and CD86 in keratinocytes derived from healthy oral mucosa and oral carcinomas. Using flow cytometry, it was confirmed that oral keratinocytes, switch on, expression of MHC class II molecules after stimulation with IFNgamma in vitro. All keratinocyte lines expressed CD40 constitutively; by contrast, CD80 and CD86 were universally absent. Loss of CD80 and CD86 may be one means whereby tumours escape immunological surveillance. (+info)Mutational escape from CD8+ T cell immunity: HCV evolution, from chimpanzees to man. (7/22)
The mechanisms by which the hepatitis C virus (HCV) establishes persistence are not yet fully understood. Previous chimpanzee and now human studies suggest that mutations within MHC class I-restricted HCV epitopes might contribute to viral escape from cytotoxic T lymphocyte (CTL) responses. However, there are several outstanding questions regarding the role of escape mutations in viral persistence and their fate in the absence of immune selection pressure. (+info)Identification of an altered peptide ligand based on the endogenously presented, rheumatoid arthritis-associated, human cartilage glycoprotein-39(263-275) epitope: an MHC anchor variant peptide for immune modulation. (8/22)
We sought to identify an altered peptide ligand (APL) based on the endogenously expressed synovial auto-epitope of human cartilage glycoprotein-39 (HC gp-39) for modulation of cognate, HLA-DR4-restricted T cells. For this purpose we employed a panel of well-characterized T cell hybridomas generated from HC gp-39-immunized HLA-DR4 transgenic mice. The hybridomas all respond to the HC gp-39(263-275) epitope when bound to HLA-DR4(B1*0401) but differ in their fine specificities. First, the major histocompatibility complex (MHC) and T-cell receptor (TCR) contact residues were identified by analysis of single site substituted analogue peptides for HLA-DR4 binding and cognate T cell recognition using both T hybridomas and polyclonal T cells from peptide-immunized HLA-DR4 transgenic mice. Analysis of single site substituted APL by cognate T cells led to identification of Phe265 as the dominant MHC anchor. The amino acids Ala268, Ser269, Glu271 and Thr272 constituted the major TCR contact residues, as substitution at these positions did not affect HLA-DR4(B1*0401) binding but abrogated T cell responses. A structural model for visualisation of TCR recognition was derived. Second, a set of non-classical APLs, modified at the MHC key anchor position but with unaltered TCR contacts, was developed. When these APLs were analysed, a partial TCR agonist was identified and found to modulate the HC gp-39(263-275)-specific, pro-inflammatory response in HLA-DR4 transgenic mice. We identified a non-classical APL by modification of the p1 MHC anchor in a synovial auto-epitope. This APL may qualify for rheumatoid arthritis immunotherapy. (+info)The symptoms of myasthenia gravis can vary in severity and may include:
* Weakness in the arms and legs
* Fatigue and muscle tiredness
* Difficulty swallowing (dysphagia)
* Difficulty speaking or slurred speech (dysarthria)
* Drooping eyelids (ptosis)
* Double vision (diplopia)
* Weakness in the muscles of the face, arms, and legs
The exact cause of myasthenia gravis is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks healthy tissues. It can also be caused by other medical conditions such as thyroid disease, vitamin deficiencies, or infections.
There is no cure for myasthenia gravis, but there are various treatments available to manage the symptoms and improve quality of life. These include:
* Medications such as corticosteroids, immunosuppressants, and cholinesterase inhibitors
* Plasmapheresis, a procedure that removes harmful antibodies from the blood
* Intravenous immunoglobulin (IVIG), which contains antibodies that can help block the immune system's attack on the nerve-muscle junction
* Surgery to remove the thymus gland, which is believed to play a role in the development of myasthenia gravis
It is important for individuals with myasthenia gravis to work closely with their healthcare provider to manage their symptoms and prevent complications. With proper treatment and self-care, many people with myasthenia gravis are able to lead active and fulfilling lives.
Thomas P. Stossel
Trogocytosis
Cowpox
Gene Shearer
Elwira Lisowska
Jung-Min Lee
List of MeSH codes (G04)
Hepatitis C virus
Trypanosomatida
T cell receptor revision
Antibiotic
CCR8 (gene)
Apolipoprotein D
GYPB
Cell (biology)
Maltose-binding protein
Alae (nematode anatomy)
Lentivirus
Autoimmunity
Exotoxin
Polysaccharide
Virus
Plasmodium falciparum erythrocyte membrane protein 1
Glycophorin A
G-quadruplex
Heparanase
Bafilomycin
Lactobacillus vaccine
Hemagglutinin (influenza)
Antibody-dependent enhancement
Immunologic adjuvant
Murine respirovirus
Natural killer cell
Blastocystosis
CD4+ T cells and antitumor immunity
Biochemical cascade
West Nile fever
Osteopontin
MYH9
PCSK9
Porcine reproductive and respiratory syndrome virus 2
Microvesicles
Heat shock protein
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Influence of the antigenicity of Brucella preparations on modulation of the immune response to sheep erythrocytes
Peptides3
- Cleavage site-specific proteases and transporter proteins involved in the processing of protein antigens into peptides also seem to play a role in the selection of antigenic peptides. (who.int)
- Efficient processing and generation of the target antigenic peptides by the UPS is essential for treatment of cancers by T-cell therapy. (academicediting.org)
- The human leukocyte antigen (HLA) system (the major histocompatibility complex [MHC] in humans) encodes cell-surface molecules which present antigenic peptides to T cells [ 4 ]. (biomedcentral.com)
Antigens5
- 1. Modulation of TL (thymus-leukemia) antigens by Fab-fragments of TL antibody. (nih.gov)
- 2. Different mechanisms for the modulation of TL antigens on murine lymphoid cells. (nih.gov)
- 3. Modulation of thymus-leukemia antigens on mouse leukemia cells induced by IgG, but not IgM, antibody. (nih.gov)
- Antigenic modulation of target antigens also reduces the therapeutic effectiveness of treatment by monoclonal antibodies. (nih.gov)
- Since most immune responses against protein and peptide antigens are T-cell dependent, the molecular target of such vaccines is to generate at least 50-100 complexes between MHC molecule and the antigenic peptide per antigen-presenting cell, sensitizing a T cell population of appropriate clonal size and effector characteristics. (who.int)
Monoclonal2
Determinants1
- 10. Common antigenic determinants in Fd fragments of guinea pig gamma 1, gamma 2 and gamma M immunoglobulins. (nih.gov)
Epitopes2
- In gene, recombinant and peptide vaccines, the immunogen is a single protein or a small assembly of epitopes from antigenic proteins. (who.int)
- The steps involved in antigen presentation and recognition by T cells that may influence the selection of antigenic protective epitopes from whole proteins will be reviewed. (who.int)
Molecular1
- Many pathogens have evolved molecular mechanisms to escape recognition by the immune system by variation of antigenic protein sequences. (who.int)
Immune responses1
- By this approach, the consequences of AhR activation on innate and adaptive immune responses to the same antigenic challenge were compared. (nih.gov)
Amino1
- Human influenza A virus (IAV) vaccination is limited by "antigenic drift," rapid antibody-driven escape reflecting amino acid substitutions in the globular domain of hemagglutinin (HA), the viral attachment protein. (nih.gov)
Receptor4
- 15. Modulation of the anti-acetylcholine receptor response and experimental autoimmune myasthenia gravis by recombinant fragments of the acetylcholine receptor. (nih.gov)
- Immune modulation by the aryl hydrocarbon receptor (AhR) has been primarily studied using 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD). (nih.gov)
- The different activation kinetics observed in soluble and immobilized enzyme versions could be due to either structural constraints to the active site conformational modulation or to a differential accessibility of the antigenic peptide (the allosteric receptor) to activating antibodies. (biomedcentral.com)
- On engagement of the T cell receptor by antigenic peptide-major histocompatibility complex (MHC) complex, a second "costimulatory" signal is critical to full T-cell activation or downregulation. (moam.info)
Cells1
- Modulation of the UPS offers been noticed and also, in particular, the phrase of the IFN- inducible components of the UPS such as PA28/ and the i-subunits 1i/LMP2 and 5i/LMP7 were found to be altered in tumor cells, affecting both the quantity and in certain cases also the quality of the generated epitopes20,21,22. (academicediting.org)
Human1
- Emphasis on antigenic responses through the immune system interaction with MNPs, modulation of human response to food and respiratory allergens, and ability of MNPs to bind and attract molecules that are harmful for humans (e.g., pathogenic microorganisms, metals, toxins). (hes-so.ch)
Response1
- Objectives To determine the anatomical location and the expression kinetics of the (+)insert SMMHC isoform in airways of horses with heaves and to evaluate its modulation in response to disease status. (bmj.com)
Effects1
- Differential Effects of Costimulatory Pathway Modulation on Corneal Allograft Survival Martin P. Watson,1 Andrew J. T. George,1 and Daniel F. P. Larkin2,3 PURPOSE. (moam.info)
Effect1
- In this study, the effect on corneal allograft survival of modulation of the costimulatory molecules programmed death-1 (PD-1) and inducible costimulatory (ICOS) molecule was examined. (moam.info)
Results1
- I. In the rabbit a repeated interaction of heterologous anti-angiotensin-converting enzyme antibodies with alveolar endothelium results in resistance to immune injury through antigenic modulation. (bvsalud.org)