Lymphokines
Macrophage-Activating Factors
Typhus, Epidemic Louse-Borne
The classic form of typhus, caused by RICKETTSIA PROWAZEKII, which is transmitted from man to man by the louse Pediculus humanus corporis. This disease is characterized by the sudden onset of intense headache, malaise, and generalized myalgia followed by the formation of a macular skin eruption and vascular and neurologic disturbances.
Interleukin-2
T-Lymphocytes
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
Chemokines, C
Lymphocyte Activation
Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.
Interferon-gamma
The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES.
Interleukin-4
Rickettsia prowazekii
Macrophage Activation
The process of altering the morphology and functional activity of macrophages so that they become avidly phagocytic. It is initiated by lymphokines, such as the macrophage activation factor (MAF) and the macrophage migration-inhibitory factor (MMIF), immune complexes, C3b, and various peptides, polysaccharides, and immunologic adjuvants.
Macrophages
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
Cytotoxicity, Immunologic
Concanavalin A
Cells, Cultured
Clone Cells
A group of genetically identical cells all descended from a single common ancestral cell by mitosis in eukaryotes or by binary fission in prokaryotes. Clone cells also include populations of recombinant DNA molecules all carrying the same inserted sequence. (From King & Stansfield, Dictionary of Genetics, 4th ed)
B-Lymphocytes
T-Lymphocytes, Helper-Inducer
Subpopulation of CD4+ lymphocytes that cooperate with other lymphocytes (either T or B) to initiate a variety of immune functions. For example, helper-inducer T-cells cooperate with B-cells to produce antibodies to thymus-dependent antigens and with other subpopulations of T-cells to initiate a variety of cell-mediated immune functions.
Interleukin-3
Interleukins
Cell Migration Inhibition
Phenomenon of cell-mediated immunity measured by in vitro inhibition of the migration or phagocytosis of antigen-stimulated LEUKOCYTES or MACROPHAGES. Specific CELL MIGRATION ASSAYS have been developed to estimate levels of migration inhibitory factors, immune reactivity against tumor-associated antigens, and immunosuppressive effects of infectious microorganisms.
Cyclosporins
A group of closely related cyclic undecapeptides from the fungi Trichoderma polysporum and Cylindocarpon lucidum. They have some antineoplastic and antifungal action and significant immunosuppressive effects. Cyclosporins have been proposed as adjuvants in tissue and organ transplantation to suppress graft rejection.
Monokines
Colony-Stimulating Factors
Glycoproteins found in a subfraction of normal mammalian plasma and urine. They stimulate the proliferation of bone marrow cells in agar cultures and the formation of colonies of granulocytes and/or macrophages. The factors include INTERLEUKIN-3; (IL-3); GRANULOCYTE COLONY-STIMULATING FACTOR; (G-CSF); MACROPHAGE COLONY-STIMULATING FACTOR; (M-CSF); and GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR; (GM-CSF).
Lymphocytes
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.
Interleukin-5
Mice, Inbred Strains
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.
Monocytes
Tuberculin
Hypersensitivity, Delayed
Antigens, Differentiation, T-Lymphocyte
Growth Substances
Lymphotoxin-alpha
A tumor necrosis factor family member that is released by activated LYMPHOCYTES. Soluble lymphotoxin is specific for TUMOR NECROSIS FACTOR RECEPTOR TYPE I; TUMOR NECROSIS FACTOR RECEPTOR TYPE II; and TUMOR NECROSIS FACTOR RECEPTOR SUPERFAMILY, MEMBER 14. Lymphotoxin-alpha can form a membrane-bound heterodimer with LYMPHOTOXIN-BETA that has specificity for the LYMPHOTOXIN BETA RECEPTOR.
Suppressor Factors, Immunologic
Proteins, protein complexes, or glycoproteins secreted by suppressor T-cells that inhibit either subsequent T-cells, B-cells, or other immunologic phenomena. Some of these factors have both histocompatibility (I-J) and antigen-specific domains which may be linked by disulfide bridges. They can be elicited by haptens or other antigens and may be mass-produced by hybridomas or monoclones in the laboratory.
Antigens, Surface
Immunity, Cellular
Phytohemagglutinins
Interleukin-1
A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation.
Dose-Response Relationship, Immunologic
Receptors, Interleukin-2
Receptors present on activated T-LYMPHOCYTES and B-LYMPHOCYTES that are specific for INTERLEUKIN-2 and play an important role in LYMPHOCYTE ACTIVATION. They are heterotrimeric proteins consisting of the INTERLEUKIN-2 RECEPTOR ALPHA SUBUNIT, the INTERLEUKIN-2 RECEPTOR BETA SUBUNIT, and the INTERLEUKIN RECEPTOR COMMON GAMMA-CHAIN.
Macrophage Migration-Inhibitory Factors
Receptors, Complement 3b
Molecular sites on or in some B-lymphocytes and macrophages that recognize and combine with COMPLEMENT C3B. The primary structure of these receptors reveal that they contain transmembrane and cytoplasmic domains, with their extracellular portion composed entirely of thirty short consensus repeats each having 60 to 70 amino acids.
Receptors, Fc
Immune Tolerance
The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc.
Interferons
Proteins secreted by vertebrate cells in response to a wide variety of inducers. They confer resistance against many different viruses, inhibit proliferation of normal and malignant cells, impede multiplication of intracellular parasites, enhance macrophage and granulocyte phagocytosis, augment natural killer cell activity, and show several other immunomodulatory functions.
Cell Division
Biological Factors
Phagocytosis
Interferon Type I
Guinea Pigs
Antibodies, Anti-Idiotypic
Immunoglobulin E
Mycobacterium bovis
Sialoglycoproteins
Receptors, Immunologic
Granulocyte-Macrophage Colony-Stimulating Factor
An acidic glycoprotein of MW 23 kDa with internal disulfide bonds. The protein is produced in response to a number of inflammatory mediators by mesenchymal cells present in the hemopoietic environment and at peripheral sites of inflammation. GM-CSF is able to stimulate the production of neutrophilic granulocytes, macrophages, and mixed granulocyte-macrophage colonies from bone marrow cells and can stimulate the formation of eosinophil colonies from fetal liver progenitor cells. GM-CSF can also stimulate some functional activities in mature granulocytes and macrophages.
Mitogens
Hybridomas
Immunization, Passive
Cytokines
Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.
RNA, Messenger
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Antigens, CD3
Complex of at least five membrane-bound polypeptides in mature T-lymphocytes that are non-covalently associated with one another and with the T-cell receptor (RECEPTORS, ANTIGEN, T-CELL). The CD3 complex includes the gamma, delta, epsilon, zeta, and eta chains (subunits). When antigen binds to the T-cell receptor, the CD3 complex transduces the activating signals to the cytoplasm of the T-cell. The CD3 gamma and delta chains (subunits) are separate from and not related to the gamma/delta chains of the T-cell receptor (RECEPTORS, ANTIGEN, T-CELL, GAMMA-DELTA).
Cycloheximide
Chemotactic Factors
Immunoglobulin M
Chemotaxis, Leukocyte
Receptors, Antigen, T-Cell
Molecules on the surface of T-lymphocytes that recognize and combine with antigens. The receptors are non-covalently associated with a complex of several polypeptides collectively called CD3 antigens (ANTIGENS, CD3). Recognition of foreign antigen and the major histocompatibility complex is accomplished by a single heterodimeric antigen-receptor structure, composed of either alpha-beta (RECEPTORS, ANTIGEN, T-CELL, ALPHA-BETA) or gamma-delta (RECEPTORS, ANTIGEN, T-CELL, GAMMA-DELTA) chains.
Histocompatibility Antigens Class II
Large, transmembrane, non-covalently linked glycoproteins (alpha and beta). Both chains can be polymorphic although there is more structural variation in the beta chains. The class II antigens in humans are called HLA-D ANTIGENS and are coded by a gene on chromosome 6. In mice, two genes named IA and IE on chromosome 17 code for the H-2 antigens. The antigens are found on B-lymphocytes, macrophages, epidermal cells, and sperm and are thought to mediate the competence of and cellular cooperation in the immune response. The term IA antigens used to refer only to the proteins encoded by the IA genes in the mouse, but is now used as a generic term for any class II histocompatibility antigen.
CD4-Positive T-Lymphocytes
A critical subpopulation of T-lymphocytes involved in the induction of most immunological functions. The HIV virus has selective tropism for the T4 cell which expresses the CD4 phenotypic marker, a receptor for HIV. In fact, the key element in the profound immunosuppression seen in HIV infection is the depletion of this subset of T-lymphocytes.
Antigens, CD8
Neoplasms, Experimental
Lymphocyte Culture Test, Mixed
Measure of histocompatibility at the HL-A locus. Peripheral blood lymphocytes from two individuals are mixed together in tissue culture for several days. Lymphocytes from incompatible individuals will stimulate each other to proliferate significantly (measured by tritiated thymidine uptake) whereas those from compatible individuals will not. In the one-way MLC test, the lymphocytes from one of the individuals are inactivated (usually by treatment with MITOMYCIN or radiation) thereby allowing only the untreated remaining population of cells to proliferate in response to foreign histocompatibility antigens.
Tetradecanoylphorbol Acetate
Interleukin-6
Killer Cells, Natural
Bone marrow-derived lymphocytes that possess cytotoxic properties, classically directed against transformed and virus-infected cells. Unlike T CELLS; and B CELLS; NK CELLS are not antigen specific. The cytotoxicity of natural killer cells is determined by the collective signaling of an array of inhibitory and stimulatory CELL SURFACE RECEPTORS. A subset of T-LYMPHOCYTES referred to as NATURAL KILLER T CELLS shares some of the properties of this cell type.
T-Lymphocytes, Cytotoxic
Immunized T-lymphocytes which can directly destroy appropriate target cells. These cytotoxic lymphocytes may be generated in vitro in mixed lymphocyte cultures (MLC), in vivo during a graft-versus-host (GVH) reaction, or after immunization with an allograft, tumor cell or virally transformed or chemically modified target cell. The lytic phenomenon is sometimes referred to as cell-mediated lympholysis (CML). These CD8-positive cells are distinct from NATURAL KILLER CELLS and NATURAL KILLER T-CELLS. There are two effector phenotypes: TC1 and TC2.
Immunoglobulin G
Tumor Necrosis Factor-alpha
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
Antigen-Presenting Cells
A heterogeneous group of immunocompetent cells that mediate the cellular immune response by processing and presenting antigens to the T-cells. Traditional antigen-presenting cells include MACROPHAGES; DENDRITIC CELLS; LANGERHANS CELLS; and B-LYMPHOCYTES. FOLLICULAR DENDRITIC CELLS are not traditional antigen-presenting cells, but because they hold antigen on their cell surface in the form of IMMUNE COMPLEXES for B-cell recognition they are considered so by some authors.
Th2 Cells
Molecular Sequence Data
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Lipopolysaccharides
Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)
Lymph Nodes
T-Lymphocyte Subsets
Gene Expression Regulation
Cell Differentiation
Base Sequence
DNA
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
Immunization
Deliberate stimulation of the host's immune response. ACTIVE IMMUNIZATION involves administration of ANTIGENS or IMMUNOLOGIC ADJUVANTS. PASSIVE IMMUNIZATION involves administration of IMMUNE SERA or LYMPHOCYTES or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow).
Inflammation
Antigens, CD
Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.
Phenotype
Tumor Cells, Cultured
VEGF is required for growth and survival in neonatal mice. (1/4704)
We employed two independent approaches to inactivate the angiogenic protein VEGF in newborn mice: inducible, Cre-loxP- mediated gene targeting, or administration of mFlt(1-3)-IgG, a soluble VEGF receptor chimeric protein. Partial inhibition of VEGF achieved by inducible gene targeting resulted in increased mortality, stunted body growth and impaired organ development, most notably of the liver. Administration of mFlt(1-3)-IgG, which achieves a higher degree of VEGF inhibition, resulted in nearly complete growth arrest and lethality. Ultrastructural analysis documented alterations in endothelial and other cell types. Histological and biochemical changes consistent with liver and renal failure were observed. Endothelial cells isolated from the liver of mFlt(1-3)-IgG-treated neonates demonstrated an increased apoptotic index, indicating that VEGF is required not only for proliferation but also for survival of endothelial cells. However, such treatment resulted in less significant alterations as the animal matured, and the dependence on VEGF was eventually lost some time after the fourth postnatal week. Administration of mFlt(1-3)-IgG to juvenile mice failed to induce apoptosis in liver endothelial cells. Thus, VEGF is essential for growth and survival in early postnatal life. However, in the fully developed animal, VEGF is likely to be involved primarily in active angiogenesis processes such as corpus luteum development. (+info)Role of alphavbeta3 integrin in the activation of vascular endothelial growth factor receptor-2. (2/4704)
Interaction between integrin alphavbeta3 and extracellular matrix is crucial for endothelial cells sprouting from capillaries and for angiogenesis. Furthermore, integrin-mediated outside-in signals co-operate with growth factor receptors to promote cell proliferation and motility. To determine a potential regulation of angiogenic inducer receptors by the integrin system, we investigated the interaction between alphavbeta3 integrin and tyrosine kinase vascular endothelial growth factor receptor-2 (VEGFR-2) in human endothelial cells. We report that tyrosine-phosphorylated VEGFR-2 co-immunoprecipitated with beta3 integrin subunit, but not with beta1 or beta5, from cells stimulated with VEGF-A165. VEGFR-2 phosphorylation and mitogenicity induced by VEGF-A165 were enhanced in cells plated on the alphavbeta3 ligand, vitronectin, compared with cells plated on the alpha5beta1 ligand, fibronectin or the alpha2beta1 ligand, collagen. BV4 anti-beta3 integrin mAb, which does not interfere with endothelial cell adhesion to vitronectin, reduced (i) the tyrosine phosphorylation of VEGFR-2; (ii) the activation of downstream transductor phosphoinositide 3-OH kinase; and (iii) biological effects triggered by VEGF-A165. These results indicate a new role for alphavbeta3 integrin in the activation of an in vitro angiogenic program in endothelial cells. Besides being the most important survival system for nascent vessels by regulating cell adhesion to matrix, alphavbeta3 integrin participates in the full activation of VEGFR-2 triggered by VEGF-A, which is an important angiogenic inducer in tumors, inflammation and tissue regeneration. (+info)Vascular endothelial growth factor activates nuclear factor of activated T cells in human endothelial cells: a role for tissue factor gene expression. (3/4704)
Vascular endothelial growth factor (VEGF) is a potent angiogenic inducer that stimulates the expression of tissue factor (TF), the major cellular initiator of blood coagulation. Here we show that signaling triggered by VEGF induced DNA-binding and transcriptional activities of nuclear factor of activated T cells (NFAT) and AP-1 in human umbilical vein endothelial cells (HUVECs). VEGF also induced TF mRNA expression and gene promoter activation by a cyclosporin A (CsA)-sensitive mechanism. As in lymphoid cells, NFAT was dephosphorylated and translocated to the nucleus upon activation of HUVECs, and these processes were blocked by CsA. NFAT was involved in the VEGF-mediated TF promoter activation as evidenced by cotransfection experiments with a dominant negative version of NFAT and site-directed mutagenesis of a newly identified NFAT site within the TF promoter that overlaps with a previously identified kappaB-like site. Strikingly, this site bound exclusively NFAT not only from nuclear extracts of HUVECs activated by VEGF, a stimulus that failed to induce NF-kappaB-binding activity, but also from extracts of cells activated with phorbol esters and calcium ionophore, a combination of stimuli that triggered the simultaneous activation of NFAT and NF-kappaB. These results implicate NFAT in the regulation of endothelial genes by physiological means and shed light on the mechanisms that switch on the gene expression program induced by VEGF and those regulating TF gene expression. (+info)Expression of vascular endothelial growth factor in human oral squamous cell carcinoma: its association with tumour progression and p53 gene status. (4/4704)
AIMS: To correlate vascular endothelial growth factor (VEGF) expression in oral squamous cell carcinoma with the clinicopathological characteristics and prognosis; and to assess whether p53 gene status is associated with VEGF expression in human cancers. METHODS: Tumour specimens from 45 patients with oral squamous cell carcinomas were examined. Expression of VEGF was determined using an immunohistochemical method, and a tumour was considered positive when more than 5% of the neoplastic cells showed VEGF immunoreactivity. The p53 gene status was screened using a polymerase chain reaction--single strand conformation polymorphism analysis. RESULTS: VEGF positive staining was detected in 19 (42.2%) of the 45 cases. VEGF immunoreactivity did not correlate with the histological degree of tumour differentiation, clinical stages, or lymph node metastasis. The patients with VEGF positive tumours had a significantly worse prognosis than those with VEGF negative tumours. The five year overall survival rate of the VEGF negative patients was 76.5%, as compared with 48.8% for the VEGF positive patients. No significant association between VEGF expression and the p53 gene status of the tumours was found. CONCLUSIONS: VEGF is a good prognostic indicator of the survival of patients with oral squamous cell carcinoma. The p53 gene status does not seem to be associated with VEGF expression in these cancers. (+info)Differential regulation of vascular endothelial growth factor and its receptor fms-like-tyrosine kinase is mediated by nitric oxide in rat renal mesangial cells. (5/4704)
Under conditions associated with local and systemic inflammation, mesangial cells and invading immune cells are likely to be responsible for the release of large amounts of nitric oxide (NO) in the glomerulus. To further define the mechanisms of NO action in the glomerulus, we attempted to identify genes which are regulated by NO in rat glomerular mesangial cells. We identified vascular endothelial growth factor (VEGF) and its receptor fms-like tyrosine kinase (FLT-1) to be under the regulatory control of exogenously applied NO in these cells. Using S-nitroso-glutathione (GSNO) as an NO-donating agent, VEGF expression was strongly induced, whereas expression of its FLT-1 receptor simultaneously decreased. Expressional regulation of VEGF and FLT-1 mRNA was transient and occurred rapidly within 1-3 h after GSNO treatment. Expression of a second VEGF-specific receptor, fetal liver kinase-1 (FLK-1/KDR), could not be detected. The inflammatory cytokine interleukin-1beta mediated a moderate increase in VEGF expression after 24 h and had no influence on FLT-1 expression. In contrast, platelet-derived growth factor-BB and basic fibroblast growth factor had no effect on VEGF expression, but strongly induced FLT-1 mRNA levels. Obviously, there is a differential regulation of VEGF and its receptor FLT-1 by NO, cytokines and growth factors in rat mesangial cells. (+info)Vascular endothelial growth factor (VEGF) receptor II-derived peptides inhibit VEGF. (6/4704)
Vascular endothelial growth factor (VEGF) directly stimulates endothelial cell proliferation and migration via tyrosine kinase receptors of the split kinase domain family. It mediates vascular growth and angiogenesis in the embryo but also in the adult in a variety of physiological and pathological conditions. The potential binding site of VEGF with its receptor was identified using cellulose-bound overlapping peptides of the extracytosolic part of the human vascular endothelial growth factor receptor II (VEGFR II). Thus, a peptide originating from the third globular domain of the VEGFR II comprising residues 247RTELNVGIDFNWEYP261 was revealed as contiguous sequence stretch, which bound 125I-VEGF165. A systematic replacement with L-amino acids within the peptide representing the putative VEGF-binding site on VEGFR II indicates Asp255 as the hydrophilic key residue for binding. The dimerized peptide (RTELNVGIDFNWEYPAS)2K inhibits VEGF165 binding with an IC50 of 0.5 microM on extracellular VEGFR II fragments and 30 microM on human umbilical vein cells. VEGF165-stimulated autophosphorylation of VEGFR II as well as proliferation and migration of microvascular endothelial cells was inhibited by the monomeric peptide RTELNVGIDFNWEYPASK at a half-maximal concentration of 3-10, 0.1, and 0.1 microM, respectively. We conclude that transduction of the VEGF165 signal can be interrupted with a peptide derived from the third Ig-like domain of VEGFR II by blockade of VEGF165 binding to its receptor. (+info)Expression of thrombospondin-1 in ischemia-induced retinal neovascularization. (7/4704)
Thrombospondin-1 is an extracellular matrix protein that inhibits endothelial cell proliferation, migration, and angiogenesis. This study was performed to investigate the role of thrombospondin-1 in ischemic retinal neovascularization. In a murine model of retinal neovascularization, thrombospondin-1 mRNA was increased from postnatal day 13 (P13), with a threefold peak response observed on P15, corresponding to the time of development of retinal neovascularization. Prominent expression of thrombospondin-1 was observed in neovascular cells, specifically, cells adjacent to the area of nonperfusion. It has been suggested that vascular endothelial growth factor (VEGF) plays a major role in ischemia-induced retinal neovascularization of this model, so we studied the effects of VEGF on thrombospondin-1 expression. In bovine retinal microcapillary endothelial cells, VEGF induced a biphasic response of thrombospondin-1 expression; VEGF decreased thrombospondin-1 mRNA 0.41-fold after 4 hours, whereas it increased, with a threefold peak response, after 24 hours. VEGF-induced endothelial cell proliferation was completely inhibited by exogenous thrombospondin-1 and increased by 37.5% with anti-thrombospondin-1 antibody. The present findings suggest that, in the ischemic retina, retinal neovascular cells increase thrombospondin-1 expression, and VEGF may stimulate endogenous thrombospondin-1 induction, which inhibits endothelial cell growth. VEGF-mediated thrombospondin-1 induction in ischemia-induced angiogenesis may be a negative feedback mechanism. (+info)Rescue of diabetes-related impairment of angiogenesis by intramuscular gene therapy with adeno-VEGF. (8/4704)
Diabetes is a major risk factor for coronary and peripheral artery diseases. Although diabetic patients often present with advanced forms of these diseases, it is not known whether the compensatory mechanisms to vascular ischemia are affected in this condition. Accordingly, we sought to determine whether diabetes could: 1) impair the development of new collateral vessel formation in response to tissue ischemia and 2) inhibit cytokine-induced therapeutic neovascularization. Hindlimb ischemia was created by femoral artery ligation in nonobese diabetic mice (NOD mice, n = 20) and in control C57 mice (n = 20). Hindlimb perfusion was evaluated by serial laser Doppler studies after the surgery. In NOD mice, measurement of the Doppler flow ratio between the ischemic and the normal limb indicated that restoration of perfusion in the ischemic hindlimb was significantly impaired. At day 14 after surgery, Doppler flow ratio in the NOD mice was 0.49+/-0.04 versus 0.73+/-0.06 for the C57 mice (P< or =0.005). This impairment in blood flow recovery persisted throughout the duration of the study with Doppler flow ratio values at day 35 of 0.50+/-0.05 versus 0.90+/-0.07 in the NOD and C57 mice, respectively (P< or =0.001). CD31 immunostaining confirmed the laser Doppler data by showing a significant reduction in capillary density in the NOD mice at 35 days after surgery (302+/-4 capillaries/mm2 versus 782+/-78 in C57 mice (P< or =0.005). The reduction in neovascularization in the NOD mice was the result of a lower level of vascular endothelial growth factor (VEGF) in the ischemic tissues, as assessed by Northern blot, Western blot and immunohistochemistry. The central role of VEGF was confirmed by showing that normal levels of neovascularization (compared with C57) could be achieved in NOD mice that had been supplemented for this growth factor via intramuscular injection of an adenoviral vector encoding for VEGF. We conclude that 1) diabetes impairs endogenous neovascularization of ischemic tissues; 2) the impairment in new blood vessel formation results from reduced expression of VEGF; and 3) cytokine supplementation achieved by intramuscular adeno-VEGF gene transfer restores neovascularization in a mouse model of diabetes. (+info)
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Edgar Pick
He co-edited the first book on lymphokines, and edited the 15 volumes of the series Lymphokines. Pick is best known for his ... While in London, Pick focused on the study of soluble products made by antigen-stimulated T lymphocytes-known as lymphokines, ... His research centered on the role of T cell-derived lymphokines in enhancing innate immunity by augmenting the capacity of ... Cohen, Stanley; Pick, Edgar; Oppenheim, Joost J. (2013). Biology of the Lymphokines. Academic Press. ISBN 978-1-4832-7142-2. " ...
Lymphokine
Lymphokines aid B cells to produce antibodies. Important lymphokines secreted by the T helper cell include: Interleukin 2 ... Lymphokines are a subset of cytokines that are produced by a type of immune cell known as a lymphocyte. They are protein ... Lymphokines at the US National Library of Medicine Medical Subject Headings (MeSH) v t e (Cytokines, All stub articles, ... Lymphokines have many roles, including the attraction of other immune cells, including macrophages and other lymphocytes, to an ...
Interleukin 16
"Modulation of lymphocyte migration by human lymphokines. II. Purification of a lymphotactic factor (LCF)". Journal of ...
Allan L. Goldstein
Thymic Hormones and Lymphokines: Their Chemistry and Clinical Applications. Plenum Press, New York, 1984. Goldstein, A.L. (ed) ...
Uromodulin
September 1987). "Uromodulin (Tamm-Horsfall glycoprotein): a renal ligand for lymphokines". Science. 237 (4821): 1479-84. ...
Cytokine
Lymphokines: produced by lymphocytes Monokines: produced exclusively by monocytes Interferons: involved in antiviral responses ... Dumonde DC, Wolstencroft RA, Panayi GS, Matthew M, Morley J, Howson WT (October 1969). ""Lymphokines": non-antibody mediators ... Cytokines have been classed as lymphokines, interleukins, and chemokines, based on their presumed function, cell of secretion, ... Cytokines include chemokines, interferons, interleukins, lymphokines, and tumour necrosis factors, but generally not hormones ...
Biofilling
The immune cells release lymphokines required for the repair and regeneration of cementum. 1. No sealability (no adhesion to ...
Granuloma annulare
Umbert, Pablo; Belcher, Richard W.; Winkelmann, R. K. (1976). "Lymphokines (MIF) in the serum of patients with sarcoidosis and ... Their data suggests that lymphokines, such as macrophage-inhibiting factor (MIF), leads to sequestration of macrophages and ...
Murine respirovirus
"Superinduction of mitogen-stimulated interferon-gamma production and other lymphokines by Sendai virus". Journal of Interferon ...
Craig B. Thompson
"CD28 activation pathway regulates the production of multiple T-cell-derived lymphokines/cytokines". Proceedings of the National ...
Interleukin
Some interleukins are classified as lymphokines, lymphocyte-produced cytokines that mediate immune responses. Interleukin 1 ...
Paraneoplastic pemphigus
The mechanism of action is by inhibiting the production of T lymphocytes and lymphokines. Cyclophosphamide is an ...
B cell growth and differentiation factors
Sherris D, Stohl W, Mayer L (April 1989). "Characterization of lymphokines mediating B cell growth and differentiation from ...
Interferon gamma
Berkowitz RS, Hill JA, Kurtz CB, Anderson DJ (January 1988). "Effects of products of activated leukocytes (lymphokines and ...
Effector cell
CIK cells respond to lymphokines by lysing tumorous cells that are resistant to NK cells or LAK cell activity. CIK cells show a ...
Wolfram Samlowski
Fowers KD, Zentner GM, Baudys M, Jurek M, Samlowski W: Formulations of lymphokines and method of use thereof for local or both ... ". "Formulations of lymphokines and method of use thereof for local or both local and systemic control of proliferative cell ...
NF-κB
RelB:p52 regulates the expression of homeostatic lymphokines, which instructs lymphoid organogenesis and lymphocyte trafficking ...
Immune system
This combination of MHC and antigen attracts a matching helper T cell, which releases lymphokines and activates the B cell. As ...
Zanvil A. Cohn
A further demonstration that macrophages could be activated by lymphokines in vivo was important in the laboratory's subsequent ... "high expectations that lymphokines and other agents interacting with macrophages would someday enter the physician's ...
RELB
... :p52 activates the expression homeostatic lymphokines, which instruct lymphoid organogenesis and determine the trafficking ...
Mycobacterium tusciae
The macrophages also carry receptors for lymphokines, and lymphokines act as cytokines which further attract T cells, B cells ...
Lymphokine-activated killer cell
LAK cells respond to these lymphokines, particularly IL-2, by lysing tumor cells that were already known to be resistant to NK ...
Cell culture
... lymphokines), and anticancer agents. Although many simpler proteins can be produced using rDNA in bacterial cultures, more ...
DNA vaccine
... lymphokines or co-stimulatory molecules. These "genetic adjuvants" can be administered as a: mixture of 2 plasmids, one ...
Macrophage
... they carry receptors for lymphokines that allow them to be "activated" into single-minded pursuit of microbes and tumour cells ... producing chemical mediators known as lymphokines that stimulate macrophages into a more aggressive form. There are several ...
GcMAF
MAFs are lymphokines that control the expression of antigens on the surface of macrophages, and one of their functions is to ...
Thomas A. Waldmann
Waldmann's research has focused on lymphokines, their receptors, and use of lymphokines and monoclonal antibodies to their ...
Cytokine-induced killer cell
CIK cells respond to these lymphokines, particularly IL-2, by lysing tumor cells that were already known to be resistant to NK ...
Minimal change disease
Rather, an altered T cell-mediated immunologic response with abnormal secretion of lymphokines by T cells is thought to modify ...
Immunosenescence
... deregulation of intracellular signal transduction capabilities diminished capacity to produce effector lymphokines shrinkage of ...
Development of specific receptors for N-formylated chemotactic peptides in a human monocyte cell line stimulated with...
... of specific receptors for N-formylated chemotactic peptides in a human monocyte cell line stimulated with lymphokines. ... When the cells are stimulated by lymphokines, however, they develop the ability both to migrate directionally and to secrete ... of specific receptors for N-formylated chemotactic peptides in a human monocyte cell line stimulated with lymphokines. Journal ...
Species-restricted effects of human and mouse lymphokines on macrophages<...
title = "Species-restricted effects of human and mouse lymphokines on macrophages",. abstract = "Lymphokines produced by ... Lymphokines produced by antigenic or mitogenic stimulation of human, guinea pig and mouse lymphocytes were tested for their ... Species-restricted effects of human and mouse lymphokines on macrophages. / Tagliabue, A.; Mantovani, A.; Boraschi, D. et al. ... N2 - Lymphokines produced by antigenic or mitogenic stimulation of human, guinea pig and mouse lymphocytes were tested for ...
Download Biology Of The Lymphokines
Prostaglandin E2 inhibits production of Th1 lymphokines but not of Th2 lymphokines. | The Journal of Immunology | American...
Prostaglandin E2 inhibits production of Th1 lymphokines but not of Th2 lymphokines. M Betz; M Betz ... M Betz, B S Fox; Prostaglandin E2 inhibits production of Th1 lymphokines but not of Th2 lymphokines.. J Immunol 1 January 1991 ... First, Th1- and Th2-associated lymphokines may be differentially sensitive to intracellular signals such as cAMP. Second, T ...
Differential immunolocalization of VEGF in rat and human adult lung, and in experimental rat lung fibrosis: light, fluorescence...
Immunologic Aspects of Organ Transplantation
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Etymologia: Cytokines - Volume 24, Number 7-July 2018 - Emerging Infectious Diseases journal - CDC
Eosinophil-lymphocyte interactions in the tumor microenvironment and cancer immunotherapy | Nature Immunology
Granuloma Annulare Medication: Corticosteroids, Retinoids, Psoralen phototherapy agents
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Hypoalbuminemia in Patients With Multiple Myeloma, Archives of Internal Medicine | 10.1001/archinte.1990.00390150095018 |...
Molecular biology of acute phase plasma proteins . Lymphokines . 1985;14:123-153. 42. Beutler B, Cerami A. Cachectin: more than ... Molecular biology of acute phase plasma proteins . Lymphokines . 1985;14:123-153. 42. Beutler B, Cerami A. Cachectin: more than ... Molecular biology of acute phase plasma proteins . Lymphokines . 1985;14:123-153. 42. Beutler B, Cerami A. Cachectin: more than ...
Excoriation Disorder Medication: Antidepressants, TCAs, Anxiolytics, Nonbenzodiazepine, Antidepressant, SSRIs, Corticosteroids,...
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Cytokines4
- Enhances immune activity through secretion of various factors, cytokines, & lymphokines. (flashcardmachine.com)
- Cytokines include interleukins, lymphokines and cell signal molecules including among others, tumor necrosis factor (TNF alpha - necrosis means killing) and interferon. (nsc24.com)
- As part of the innate immune system, inflammasomes play an important role in the induction of inflammatory cascades and coordination of host defenses, via the activation and secretion of pro-inflammatory cytokines (chemokines, interferons, interleukins, lymphokines, and tumor necrosis factors). (dadamo.com)
- It does this by secretion of lymphokines and cytokines, among them interleukin-2 and interferon, which act as 'messengers' to tell specific cells to attack and destroy invading pathogens. (lifeextension.com)
Interferons2
- The cytokine group of proteins includes lymphokines, interferons, colony stimulating factors and chemokines. (sigmaaldrich.com)
- 1987) in Lymphokines and Interferons, a Practical Approach. (bio-techne.com)
Inhibitory2
- Clobetasol affects the production of lymphokines and has inhibitory effects on Langerhans cells. (medscape.com)
- The results indicated that guinea- pig lymphoid cells produced two inhibitory lymphokines along with HRF upon stimulation with antigens or mitogens. (cdc.gov)
Macrophages2
- Lymphokines produced by antigenic or mitogenic stimulation of human, guinea pig and mouse lymphocytes were tested for their effects on monocytes or macrophages of the same and heterologous species, to determine whether there is any species restriction in their reactivity. (elsevier.com)
- Other immune cells that battle malignant cells are macrophages, antigen-presenting cells, and substances produced by immune cells called lymphokines. (howstuffworks.com)
Lymphocyte1
- Lymphokines": non-antibody mediators of cellular immunity generated by lymphocyte activation. (cdc.gov)
Hormones1
- Suppressor T cells are sensitive to high concentrations of circulating lymphokine hormones, and release their own lymphokines after an immune response has achieved its goal. (medicinenet.com)
Production3
- Prostaglandin E2 inhibits production of Th1 lymphokines but not of Th2 lymphokines. (aai.org)
- It kills cancer cells and caused the production of lymphokines. (ecopolitan.com)
- CsA has been found to inhibit the immune responses mediated by the production and release of T-cells and lymphokines. (siemens-healthineers.com)
Cells3
- When the cells are stimulated by lymphokines, however, they develop the ability both to migrate directionally and to secrete enzymes in response to several types of chemoattractants. (duke.edu)
- Immune function is also under the powerful influence of PGE-1, which controls the release of lymphokines known to activate immune system cells. (prohealth.com)
- Interleukin 2 (IL-2), one of the most important lymphokines secreted by activated helper T-cells, plays a pivotal role in the generation and regulation of the immune response. (uottawa.ca)
Cell1
- Development of specific receptors for N-formylated chemotactic peptides in a human monocyte cell line stimulated with lymphokines. (duke.edu)
Activity1
- All three lymphokines were detected in most supernatants and the final activity of the supernatant elected the predominant factor present. (cdc.gov)
Interleukins1
- In cellular immunity, helper T-lymphocytes play a role via the lymphokines they secrete (interleukins, interferon, and tumor necrosis factor-beta (TNF- β )), whereas macrophages play a role via the reactive oxygen metabolites, and nitric oxide plays a role by means of various enzymes and lymphokines such as TNF- α [ 4 ]. (hindawi.com)
Proteins4
- Cell lineages especially important to the immune response include two classes of lymphocytes: B-cells, which can produce and secrete immunoglobulins (proteins with the capability of recognizing and binding to foreign matter to effect its removal), and T-cells of various subsets that secrete lymphokines and induce or suppress the B-cells and various other cells (including other T-cells) making up the immune network. (justia.com)
- In addition to increasing the ability of the macrophages to engulf and destroy cancer cells, microbes, and other foreign cells, the beta-glucan binding stimulates production of signalling proteins in the immune system such as interleukin-1, interleukin-2, and lymphokines, which ramp up defences by activating immune cells. (alive.com)
- The function of cells involved in this process is controlled by the cell membrane activation of intracellular translational pathways interacting with the nucleus that produces transcriptional proteins, which control cellular behavior such as secretion of lymphokines or cell proliferation. (novapublishers.com)
- Lymphokines are proteins that communicate with other cells and help to coordinate the immune response. (friendlyfarms.cc)
Tumour necros1
- These exotoxins act as "superantigens" by stimulating large numbers of T cells to release lymphokines (interleukin 2, tumour necrosis factor). (bmj.com)
Lymphocytes7
- Cyclosporine acts specifically and reversibly on T-lymphocytes and inhibits the antigen-triggered release of lymphokines by activated T-cells. (lambertvetsupply.com)
- Stimulation of B lymphocytes by antigen and the appropriate lymphokines induces the production of a different Ig isotypes while maintaining the same antigen-binding specificity. (nih.gov)
- Arrows on Basal Membrane -- Reaction of the airways to an antigen begins within 15 minutes after exposure, when inflammatory lymphokines and IgE-binding factors are secreted from T-lymphocytes. (uab.edu)
- It is a transmembrane molecule with 7 potential N-glycosylated sites, expressed on resting monocytes and endothelial cells and can be upregulated on many other cells, e.g. with lymphokines, on B- and T-lymphocytes, thymocytes, dendritic cells and also on keratinocytes, chondrocytes, as well as epithelial cells. (exbio.cz)
- Exudative-sensitized lymphocytes in tuberculous pleural fluid reacted to the specific antigen more effectively and produced higher titers of lymphokines including interferon gamma (IFN-gamma) and interleukin 2 (IL-2) than circulating lymphocytes. (nagoya-u.ac.jp)
- Thus, activated T-lymphocytes involve the production of lymphokines at the morbid site and they effectively exert local cellular immunity through the action of such lymphokines. (nagoya-u.ac.jp)
- If T-lymphocytes recognize foreign or modified-self cell structures they start producing different mediators, so-called lymphokines, such as interferon-γ. (gotomydoctor.com)
19871
- 1987. Lymphokines 13:151. (biolegend.com)
19842
- and , Lymphokines 1984. (crossref.org)
- Throughout the Second Red Scare, the download Thymic Hormones and Lymphokines: Basic Chemistry and Clinical Applications 1984 of the ' administrative area ' run itself as an liberties--to and a subject to the United States in a following philosophical compatibility. (hsunet.com)
Antigen2
- Mg participates in immune responses in numerous ways: as a cofactor for immunoglobulin synthesis, C'3 convertase, immune cell adherence, antibody-dependent cytolysis, IgM lymphocyte binding, macrophage response to lymphokines, T helper-B cell adherence, binding of substance P to lymphoblasts and antigen binding to macrophage RNA. (nih.gov)
- This mixture of MHC and antigen attracts an identical helper T cell, which releases lymphokines and prompts the B cell. (badmintonandalucia.com)
Secrete1
- Thus, intratumor accumulation requires stronger stimulation than for proliferation or the capacity to secrete lymphokines. (aacrjournals.org)
Mediators1
- Lymphokines': molecular mediators of cellular immune responses in animals and man. (nih.gov)
Hormones1
- Among a panel of lymphokines and growth hormones, only human GM-CSF could compete for binding of human 125I-GM-CSF to these cells. (rupress.org)
Secretion1
- Also mediates the secretion of important lymphokines. (nih.gov)
Macrophage1
- 17. The role of plasma membrane receptors and the kinetics of macrophage activation by lymphokines encapsulated in liposomes. (nih.gov)
Induce1
- These changes regulate cellular movements and lead to activation of transcriptional events that induce production of T cell lymphokines and result in differentiative events. (nih.gov)
Cellular2
- Lymphokines apparently mediate cellular activities in a variety of ways. (justia.com)
- The different cellular lineages often respond in a different manner when lymphokines are administered in conjunction with other agents. (justia.com)
Synthesis1
- a substantial increase in collagen synthesis is triggered by lymphokines from patients with idiopathic pulmonary fibrosis. (bmj.com)
Initiate1
- This prevents the dephosphorylation and translocation of nuclear factor of activated T-cells (NF-AT), a nuclear component thought to initiate gene transcription for the formation of lymphokines. (aksci.com)
Human2
- 3. Intravenous, intralesional and endolymphatic administration of lymphokines in human cancer. (nih.gov)
- Human Lymphokines, "Pre-Clinical and Phase I Clinical Trials with Lymphotoxin," 1982, pages 621 through 629. (ipmall.info)
Effects1
- Lymphokines in nanomolar to picomolar concentra- tons cause profound enhancing or suppressing effects on the label claim. (themauimiracle.org)