Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P14784 (IL-2 receptor)
 3,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effective stimulation of CD4+ T cells in an immune response depends on activation signals transduced via not only the CD3-T-cell receptor (TCR) complex but also those generated by accessory cell-surface proteins, including some that mediate adhesion between T cells and antigen-presenting cells (APC). Three members of the Ig superfamily, CD54 [intercellular cell adhesion molecule 1 (ICAM-1)], CD58 [lymphocyte function-associated antigen 3 (LFA-3)], and B7, expressed on the surface of APC, have been shown to mediate both adhesion and signaling during T cell-APC interactions. Recently another member of the Ig superfamily, [vascular cell adhesion molecule 1 (VCAM-1; INCAM110)], has been identified. VCAM-1 mediates adhesion between endothelial cells and activated lymphocytes and certain tumor cells. Here, using a soluble VCAM-1 fusion protein with receptor globulin (Rg), we examined the role of VCAM-1 in T-cell activation. We observed that CD4+ T cells, which are inefficiently stimulated by immobilized anti-TCR-1 or anti-CD3 monoclonal antibody (mAb) alone, can be induced to proliferate when exposed to immobilized VCAM-1-Rg in conjunction with either immobilized anti-TCR-1 or immobilized anti-CD3 mAb. The costimulatory effects of VCAM-1-Rg on CD4+T cells is inhibited by mAb to either the CD29 (integrin beta 1)-CD49d [very late activation antigen 4 alpha (VLA-4 alpha)] complex on the surface of CD4+ T cells or to VCAM-1. Stimulation of CD4+ T cells with immobilized VCAM-1-Rg and anti-TCR or -CD3 mAb results in the synthesis of both interleukin 2 (IL-2) receptors and IL-2. In addition, anti-CD25 (anti-IL-2 receptor a) mAb significantly inhibited the VCAM-1-Rg/anti-TCR or -CD3 mAb-driven activation of CD4+ T cells, indicating that endogenously produced IL-2 is in part responsible for the observed T-cell proliferation. Collectively, these results suggest that VCAM-1 can play an important costimulatory role during the activation of CD4+ T cells.
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PMID:Vascular cell adhesion molecule 1 induces T-cell antigen receptor-dependent activation of CD4+T lymphocytes. 171 78

Although alterations in T lymphocyte subset distribution and function in the peripheral blood of HIV-infected humans are well defined, the extent to which these reflect changes in other lymphoid compartments is unclear. We have characterized the coincident changes in PBL and lymph nodes (LN)1 after simian immunodeficiency virus of macaques (SIVmac) infection of rhesus monkeys. Whereas no consistent change in CD8+ PBL was noted during the first 60 d after infection, CD8+ lymphocytes increased significantly in number in LN. These CD8+ LN lymphocytes exhibited an increased expression of MHC class II and a decreased expression of leukocyte adhesion molecule-1, suggesting that they were activated, but interestingly did not express CD25 (IL-2 receptor). Moreover, there was no evidence that these CD8+ LN cells were proliferating, suggesting that they had migrated to the LN. These changes in the LN CD8+ lymphocyte population preceded any detectable change in the light microscopic appearance of the LN. When SIVmac-specific effector T cell responses were assessed, the magnitude of virus-specific effector activity was nearly identical in the PBL and LN of each monkey studied. However, the presence of SIVmac-specific effector cells in the LN did not correlate with the presence of CD8+, MHC class II+ cells. These findings suggest that this numerically important CD8+ lymphocyte subpopulation may serve a regulatory function.
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PMID:An activated CD8+ lymphocyte appears in lymph nodes of rhesus monkeys early after infection with simian immunodeficiency virus. 171 8

A number of markers which have been proposed to identify B cell subsets have been reassessed on human B cells, using an immunofluorescence technique optimized for sensitivity and an analytical mode which yields histograms showing the distribution of fluorescence on B cells. The results show that CD38, CD22, CD23, FMC6, and anti-IgM react with all blood B cells, albeit with a broad and complex distribution of fluorescence. CD5, CD9, CD10, CD43, and IgD can be regarded as subset markers since they give clearly bimodal distributions of fluorescence intensity. CD5 staining showed at least three populations, with a small number (3-5 per cent) of cells brightly stained and a population of variable size staining weakly. No clearly defined populations were seen with CD45R0, although staining was slightly above background. An antibody against the LAM-1 molecule reacted with all blood B cells. Expression of the IL-2 receptor p55 chain (CD25) was clearly bimodal, whereas the p75 chain was essentially negative on B cells. The relationship between subsets in blood and subsets in tissue, and between subsets identified by different markers in blood, is discussed.
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PMID:The expression of sub-population markers on B cells: a re-evaluation using high-sensitivity fluorescence flow cytometry. 172 68

The primary tumour cells and tumour infiltrating lymphocytes (TILs) of 31 breast cancer patients have been analysed by dual colour flow cytometry to determine whether the phenotype and/or activation status of the TILs bears any relationship to the expression of MHC antigens on the tumour cells. The phenotype and activation status of 5000 TILs were studied using Mabs to CD4, CD8, HLA DR, CD25 (the low affinity inducible IL-2 receptor) and the transferrin receptor and related to Class I and Class II MHC expression on 5000 primary tumour cells. On the tumour cells, Class I MHC expression ranged from 1-74%, averaging 12.9%. HLA DR expression ranged from 1-69% averaging 14.3%. When the phenotypic proportions of the lymphocytic infiltrate were analysed there was found to be a correlation between tumour expression of Class I MHC and the proportion of both CD4+ (P less than 0.05) and CD8+ (P less than 0.02) T cells within the tumour. No such relationship was found with the MHC Class II antigen. When TIL activation markers were analysed, the percentage of CD8+ TILs positive for HLA DR expression correlated strongly with the expression of Class I (P less than 0.001) and Class II (P less than 0.001) antigens on the tumour cells. The percentage of CD4+ TILs positive for HLA DR expression also correlated significantly, but less strongly with the expression of Class I (P less than 0.01) and Class II (P less than 0.02) antigen expression on the tumour cells. The percentage of CD4+ TILs positive for CD25 expression correlated with both Class I (P less than 0.05) and Class II (P less than 0.03) expression on the tumour cells while the percentage of CD8+ TILs positive for CD25 did not. The percentage of TILs bearing the transferrin receptor showed no measurable correlation with the expression of either class of MHC antigen on the tumour. The data suggest that MHC expression on the tumour cells has a selective effect on the response capacity of different parts of the immune system.
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PMID:Flow cytometric analysis of tumour infiltrating lymphocyte activation and tumour cell MHC class I and II expression in breast cancer patients. 173 Jan 39

The immunological study of the major histocompatibility complex (class I, class II and DR antigens), tumour infiltrating lymphocytes (TIL), regional lymph node lymphocytes (RLNL) and peripheral blood lymphocytes (PBL) was evaluated on the basis of immunohistochemical staining using monoclonal antibodies of each subset of lymphocytes in a series of 16 patients with renal cell carcinoma. Two renal cell carcinomas in dialysis patients with acquired cystic disease of the kidneys (ACDK) were also included in this study. With regard to the immunological environment, a comparative study between renal cell carcinoma accompanied with ACDK and 14 other renal cell carcinoma was carried out. The results are described below: 1) With regard to the expression of MHC antigens in tumour cells, the degrees of expression of MHC class I, class II and DR-antigen in case 1 were higher than that of the other 14 renal cell carcinomas. On the other hand, no expression of MHC was detected in case 2. 2) As to the subsets of TIL, the CD25 (IL-2 receptor) was not expressed in all the renal cell carcinoma. As to the T cell receptor (TCR-alpha/beta chain), the degree of expression was the same in case 1 and the other 14 cases. On the other hand, no TCR was detected in the case 2. As to the other subsets of TIL (CD3, CD4, CD8, CD16 and CD20), the rates of the infiltration were the same in case 1 and the other 14 cases, but those in case 2 were lesser than in all other 14 cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunological study on renal cell carcinoma in dialysis patients with acquired cystic disease of kidneys]. 176 69

Ficoll-separated and monocyte-depleted mononuclear cells isolated from normal leukapheresis products were cryopreserved. These cells were incubated with or without 1,000 U/ml of recombinant interleukin-2 (rIL-2) for 4 days, and their lymphokine-activated killer (LAK) and natural killer (NK) activities were measured. IL-2 activation induced a significant increase in the expression of the CD25 antigen. There was no change in CD2, CD3, CD4, CD8, CD16, CD56 and CD57 cell marker expression. Cryopreservation did not induce any change in the membrane antigen expression and in the lymphocyte subsets. The NK activity was well preserved and the decrease of LAK activity of IL-2-activated cells after cryopreservation was not significant. In contrast, cells activated before cryopreservation had a significantly lower cytotoxic activity and the number of cells expressing the IL-2 receptor was also significantly reduced. However, the decrease of CD56 expression was not significant. CD25 expression seemed to be proportional to the LAK activity of the cells. This study demonstrated that cryopreserved lymphocytes, after 4 days of culture with rIL-2, could be as active and could express the CD25 and CD56 cell surface markers in the same manner as fresh LAK cells.
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PMID:The influence of cryopreservation on activity and surface markers of lymphokine-activated killer cells. 176 4

During the last few years, several observations outline that the impaired T lymphocyte proliferative capacity in the elderly is due to a reduced interleukin 2 (IL-2) release. To further investigate the activation process during lectin stimulation, aged peripheral blood mononuclear cells (PBMC) were stimulated with phytohemagglutinin (PHA) and assessed for CD25 (IL-2 receptor) and CD71 (transferrin receptor) expression at different intervals of time. Our results provided evidence for a significant decline of both structure induction, above all in the later phase of culture. Indomethacin (INDO) treatment gave rise to an enhancement of CD71 antigen expression only, while prostaglandin E2 (PGE2) supplementation to culture media further decreased either CD25 or CD71 receptor induction. Interferon (IFN)-alpha and IFN-gamma treatment failed to modulate the frequency of CD25+ and/or CD71+ cells. Finally, the expression of CD71 receptor was increased by deferoxamine supplementation, this suggesting a partial involvement of iron overload in the depressed function. Although further studies are required to evaluate at a molecular level the decreased antigen expression, these findings indicate that several mechanism are involved in the elderly-related decline of T lymphocyte activation structures during lectin stimulation.
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PMID:Modulating effects on CD25 and CD71 antigen expression by lectin-stimulated T lymphocytes in the elderly. 177 Feb 20

The extracellular matrix (ECM) is composed of a number of macromolecules that promote cell adhesion, cell migration, and differentiation. Receptors for these molecules have been identified and belong to a superfamily of cell surface proteins, collectively known as the integrins. In this study, we show that the matrix protein fibronectin (FN) acts synergistically with immobilized anti-CD3 antibody to promote proliferation of total human peripheral blood lymphocytes (HPBL) in the absence of exogenous IL-2. Proliferation was inhibited by both the alpha 5 beta 1 and alpha 4 beta 1 recognition peptides. ARG-GLY-ASP (RGD), and GLU-ILE-LEU-ASP-VAL-PRO-SER-THR (EILDVPST), respectively. Expression of CD25 (IL-2 receptor) was significantly higher on cells cultured on anti-CD3 and FN, indicative of T-cell activation. Additionally, cells cultured on immobilized anti-CD3 and FN for 3 days showed increased adhesion to FN and increased forward light scatter/side scatter profile. Synthesis of both IL-1 and to a lesser extent IL-2 was elevated in supernatants from cultures containing both anti-CD3 and FN. These data are consistent with published reports which demonstrate that ECM proteins can act as costimulants of lymphocyte proliferation. Finally, our results show that cells cultured on anti-CD3 antibody and FN have an activated phenotype and that cytokines may be involved in this process.
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PMID:Fibronectin augments anti-CD3-mediated IL-2 receptor (CD25) expression on human peripheral blood lymphocytes. 182 61

Staphylococcal enterotoxins are able both to stimulate powerful polyclonal proliferative responses and to induce non-responsiveness of T lymphocytes expressing the appropriate T-cell antigen receptor V beta gene products. T-cell clones representative of the human response to house dust mite were identified that express either V beta 3 or V beta 6 gene products. The specificity of the latter was confirmed by serology. Pre-treatment of cloned V beta 3+ T cells with the Staphylococcus aureus enterotoxins B or C1 rendered them non-responsive to immunogenic challenge with their natural ligand, while retaining responsiveness to exogenous IL-2. Similarly, exposure of the V beta 6+ dust mite reactive T cells to the staphylococcal enterotoxin of the appropriate specificity, SEE, induced specific anergy. The development of non-responsiveness was associated with changes in the T-cell phenotypes. Downregulation of the T-cell receptor, Ti-CD3, was paralleled by enhanced expression of both CD2 and the IL-2 receptor, CD25. Differential co-modulation of CD4 and Ti-CD3 suggested that for some T cells CD4 may form part of the specific antigen recognition structure. Toxicity of the staphylococcal enterotoxins may be removed by chemical modification, thus their ability functionally to inactivate subpopulations of T cells expressing antigen-specific receptors with shared characteristics may be of potential value in the regulation of allergic diseases if the diversity of the T-cell repertoire proves to be limited.
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PMID:Functional inactivation of Dermatophagoides spp. (house dust mite) reactive human T-cell clones. 182 87

Significant proliferative responses of peripheral blood mononuclear cells (PBMC) to crude Plasmodium falciparum schizont antigen (M.Ag) or purified recombinant 31.1 Ag (part of gp 195) were observed only in 46 and 39%, respectively, of 50 healthy subjects 5 to 63 years old living in Gabon, a malaria-endemic area. High responses to pokeweed mitogen were observed in all the subjects except one. Interferon-gamma (IFN-gamma) production paralleled the proliferative response, but in some subjects proliferation without a IFN-gamma response was observed. The proportion of subjects responding to M.Ag and 31.1 Ag increased with age. By cytofluorometric analysis performed with PBMC from 27 subjects, a substantial proportion of CD3+ T cells was found to bear the activation marker HLA-DR. However, the CD3+ cells expressed very low levels of CD25 (p55 chain of IL-2 receptor). The expression of CD25 on T cells and their capacity to respond to M.Ag were significantly correlated. In four subjects an increase in the percentage of CD3+ cells bearing the very late activation marker VLA-1 was observed.
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PMID:In vivo decreased expression of CD25 (p55 chain of IL-2 receptor) on CD3+ T cells correlates with low in vitro responsiveness to Plasmodium falciparum antigen in subjects living in a malaria endemic area. 182 93


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