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)

Expression of CD4, CD8, IL-2 receptor alpha chain (IL-2R alpha), and MHC class II (MHC-II) on peripheral blood mononuclear cells were examined in cats infected with feline immunodeficiency virus (FIV). CD4/CD8 T cell ratio in FIV-infected cats was slightly decreased, as compared with that in specific-pathogen-free (SPF) cats. However, there was no statistical differences between them. The number of circulating IL-2R alpha+ cells in FIV-infected cats was higher than that in healthy cats, whereas induction of IL-2R alpha expression by concanavalin A (Con A) stimulation was depressed in FIV-infected cats. By using two-color cytofluorometry, Con A-induced enhancement of IL-2R alpha expression was found to be reduced in both CD4+ and CD8+ populations in PBMC from FIV-infected cats. The circulating MHC-II+ cells were also increased in FIV-infected cats. Furthermore, the induction of IL-2R alpha expression on PBMC after Con A-stimulation significantly depressed by FIV inoculation in vitro. These results suggest that FIV activates PBMC in vivo via direct and/or indirect mechanisms, leading to the unresponsive state of T cells to further stimuli in vitro.
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PMID:Altered surface antigen expression on peripheral blood mononuclear cells in cats infected with feline immunodeficiency virus. 132 15

The bacterial exotoxins staphylococcal enterotoxin A and B (SEA and SEB) mediate disease through their effects on T lymphocytes. In this manuscript we have demonstrated that both SEA and SEB can directly activate purified T cells in the absence of accessory cells as determined by a transition from G0 to G1 and induction of IL-2 receptor expression. However, neither SEA nor SEB alone was sufficient to result in T-cell proliferation. The induction of T-cell proliferation by SEB or SEA required the addition of a second costimulatory signal. This could be provided by either accessory cells or monoclonal antibody stimulation of CD28. As previously reported, T-cell proliferation induced by enterotoxin in the presence of accessory cells was partially inhibited by a blocking antibody against class II MHC. In contrast, in purified T cells when costimulation was provided through CD28, proliferation was not inhibited by class II antibody, and HLA-DR expression was not detectable. In addition, costimulation through CD28 was partially resistant to the effects of cyclosporin A. These results demonstrate that CD28 costimulation is sufficient to induce proliferation of enterotoxin-activated T cells, and that this effect is independent of class II MHC expression.
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PMID:CD28 and staphylococcal enterotoxins synergize to induce MHC-independent T-cell proliferation. 133 Mar 29

The Fc gamma RIII receptor (CD16) has been described on natural killer cells and a small subset of T lymphocytes. CD16+bright lymphocytes represent the typical population of peripheral blood CD3- NK cells. In these studies in addition to CD16+bright NK cells Fc gamma RIII expressing cytotoxic T lymphocytes in peripheral blood from one healthy individual are characterized as CD16+dim non-MHC-restricted CTLs either expressing the alpha/beta (80%) or the gamma/delta T cell receptor (20%). Both CD16+ subsets are clearly distinct in their functional capacity performing NK and ADCC activity. Freshly isolated CD16+dim T cells exert higher ADCC, CD16+bright NK cells higher NK activity. They are also differentially activated by interleukin-2 since CD16+bright NK cells reveal a bright expression of the p75 IL-2 receptor beta-chain in contrast to the very low p75 expression on CD16+dim T cells. This activation leads to a gradual increase of ADCC by NK cells. Finally the CD16 expression pattern with low and bright intensity represents a stable phenotype expressed by clones generated from these different subpopulations. On a clonal level CD16+dim non-MHC-restricted T cells can be distinguished from CD16+bright NK cells by their lower capacity in NK killing, but they are equally potent in ADCC. Finally these CD3+CD16+dim clones provide the basis for studies of Fc gamma RIII and TcR interaction.
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PMID:Analysis of CD16+dim and CD16+bright lymphocytes--comparison of peripheral and clonal non-MHC-restricted T cells and NK cells. 139 40

Analysis of peripheral blood lymphocytes by two- and three-colour high-sensitivity staining with UCHL1 (CD45RO) and other markers shows that the expression of CD45RO on lymphocyte subsets is more complex than is generally supposed. In addition to the populations which express CD45RO and RA in a mutually exclusive manner, up to 30% of cells in adult blood express both markers, at low levels. This "intermediate" population includes CD4-positive cells, and a proportion of these cells express the p55 chain of the IL-2 receptor (CD25), suggesting that they are activated. In cord blood there are few RO-bright cells, but CD45RO is expressed at low intensity on a proportion of cells. Among the CD45RO-bright cells in adult blood at least two subsets can be detected by using MHC Class II and the homing receptor L-selectin as additional markers. This complexity suggests that memory cells are a subset of CD45RO-expressing cells, but that this marker is also found on cells that are activated but not irreversibly "switched" to memory cells.
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PMID:The CD45RO (p180, UCHL1) marker: complexity of expression in peripheral blood. 142 42

Molecular interaction and transmembrane signal transducing events generate a very dynamic and ever changing "pattern" in the plasma membranes. Lymphocytes, the key functional elements of the immune system, are eminently suited to be the primary targets to investigate these proximity, mobility, or other physical-chemical changes in their plasma membranes. Recently, a number of experiments suggested that processed peptides from antigens can bind specific components of MHC molecules (Elliott et al., 1991). This is certainly a way to alter their structure. Cell surface patterns of topological nature, assembly and disassembly of oligomeric receptor structure like the IL-2 receptor have been investigated by sophisticated biophysical techniques. The dynamic changes in the two-dimensional cell surface pattern and intramolecular conformational changes within this "larger" macro-pattern may have a strong regulatory role in signal transducing and intercellular recognition processes. Recent data on these problems are presented together with brief and critical discussions.
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PMID:Dynamic physical interactions of plasma membrane molecules generate cell surface patterns and regulate cell activation processes. 145 9

We studied the expression of class II MHC product (HLA DR) and IL-2 receptor on circulating monocytes (M phi) in MS patients, neurological and healthy controls, by double color flow cytometry. In all groups most M phi were DR+ without significant differences. More interesting, low percentages of IL-2+ M phi were detectable in healthy and neurological controls, whilst a few MS patients with active disease showed higher levels. This finding is in agreement with similar studies in other T-cell mediated diseases and with the report of rare IL-2+ macrophages in MS plaques. Although the actual role of IL-2+ M phi in the immune response still needs elucidation, our findings suggest their relevance to the pathological process of demyelinating disease.
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PMID:Interleukin-2 receptor expression on blood monocytes of patients with multiple sclerosis. 147 48

Several studies have reported a suppressed immune function (e.g. blast transformation) during depression. In an attempt to define the cellular basis of the reported immune disorders, the present study investigates the leukocyte cell subset profile of minor, simple major, and melancholic depressives, versus normal controls. We have counted the number of white blood cells (WBC) lymphocytes, monocytes, and granulocytes, while the number of lymphocyte (sub)populations has been identified by phenotype, using monoclonal antibody staining in conjunction with flow cytometry. The following cell surface antigens were determined: CD3+ (pan T), CD19+ (pan B), CD4+ (T helper/inducer), CD8+ (T suppressor/cytotoxic), CD4+CD45RA (T-memory cells), CD4+CD45RA+ (T-virgin cells), surface Ig, class II MHC HLA-DR, and CD25+ (IL-2 receptor). By means of pattern recognition methods, we established distinct immunological changes in minor and simple major depressed and in melancholic patients, setting them apart from the reference population. Depression, per se, is characterized by a higher number of WBC, monocytes, class II MHC HLA-DR, and memory T cells. Minor and simple major depressives exhibited an increased T helper/suppressor ratio. Increased numbers of IL-2 receptor bearing cells are a hallmark for major depression. Melancholics showed an increased number of pan T, pan B and T suppressor/cytotoxic cells. It was concluded that the established immune cell profile of depressed patients may point towards the existence of a systemic immune activation during that illness.
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PMID:Evidence for a systemic immune activation during depression: results of leukocyte enumeration by flow cytometry in conjunction with monoclonal antibody staining. 157 66

IL-2 receptor positive T-cells from leukocyte-infiltrated pancreatic islets of diabetes prone or acutely diabetic NOD mice were propagated in vitro by culture in interleukin-2 containing medium. Of 13 lines obtained after limiting dilution all were positive for the T-cell marker Thy-1 and for CD8. Considerable heterogeneity in T-cell receptor usage was noted. Seven lines expressed T-cell receptors using V beta 8, one line was positive for V beta 5 and two lines expressed a non V beta 5, non V beta 8 receptor. Finally, two further lines lacked T-cell receptors. None of the cell lines were cytotoxic to islet cells although 10 lines showed non MHC restricted lysis of one or more tumour cells including rat insulinoma cells. We conclude that IL-2 receptor positive CD8+ T-lymphocytes from NOD islets are heterogenous with respect to V beta T-cell receptor usage. The majority of these cells are not cytotoxic to islet cells.
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PMID:Analysis of IL-2 receptor positive CD8(+)-T-lymphocytes grown from islets of NOD mice. 168 10

Both CD3- and CD3+ CD56+ effector cells can mediate non-MHC-restricted lysis in the absence of activation. Previous studies have shown that both of these subsets can be augmented with IL-2. In the present study, we have examined further the phenotypic markers expressed on these cells as well as the functional capacities of these subsets, including LAK activity, cytokine expression, and pore-forming protein (PFP) production. In addition, these populations were analyzed for clonality by Southern blot analysis of the T cell receptor beta chain gene constant region. The CD3-, CD56+ and CD3+, CD56+ lymphocytes were quite similar in their phenotypic markers, although the CD3+, CD56+ lymphocytes lacked high levels of IL-2 receptor beta chain and did not express CD16. The CD3+, CD56+ lymphocytes mediated non-MHC-restricted lysis, but failed to express LAK activity or be induced by IL-2 to secrete IFN gamma, a characteristic of the CD3-, CD56+ lymphocytes. The T cell receptor beta chain gene pattern of the CD3+, CD56+ lymphocytes was characteristic of a polyclonal cell population. Of interest, both populations of cells appeared morphologically to be large granular lymphocytes that contain PFP in their cytoplasmic granules. Therefore these CD56+ subsets provide a new model to study several questions related to non-MHC-restricted target cell lysis, including the identification of novel receptors involved in target cell recognition and/or triggering as well as the biochemical pathways implicated in cellular lysis.
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PMID:Comparative studies of CD3- and CD3+ CD56+ cells: examination of morphology, functions, T cell receptor rearrangement, and pore-forming protein expression. 171 95

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


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