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)

Human cell lines (the T-cell lines H9, Jurkat, and HUT102, the myeloid lines U937 and HL60, and the Raji B cell line) were infected with HIV-1. HIV-1 antigen could be detected by immunofluorescence analysis in more than 50% of T cells and myeloid cells 15 days after infection. Infection of Raji cells took more than 2-3 months. Studies of cell surface marker expression revealed remarkable changes after HIV-1 infection of Raji cells: expression of CR2 (C3d/EBV receptor, CD19, CD20, CD22, CD23, CD10, and surface IgM) were highly reduced, in the case of CR2 and membrane-IgM from 100 to 0%, whereas levels of CD37 and CD38 remained unaltered by HIV-1 infection. U937 cells showed a reduction of CD4 expression from 14 to 5% after HIV-1 infection; the CR3 expression slightly increased from 25 to 30%. In contrast, HLA-DR was only expressed (21%) after HIV-1 infection but not in uninfected U937 cells. Expression of HLA-DR could be detected also in HL60 cells (33%) after HIV-1 infection. In H9 cells, CD4 was reduced from 60 to 30% after HIV-1 infection, whereas HLA-DR and CD25/IL-2 receptor expression increased from 16 to 90% and from 0 to 50%, respectively. CD4 was reduced from 70 to 0% from Jurkat cells after HIV-1 infection, whereas expression of CR2 was only slightly diminished from 8 to 4%. Expression of CR1 and HLA-DR was slightly increased in these cells (1 to 3%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression of the C3d/EBV receptor and of other cell membrane surface markers is altered upon HIV-1 infection of myeloid, T, and B cells. 213 11

A 36-year-old man presented with an acute immune-mediated illness characterized by leukocytoclastic vasculitis and polyarthritis. Evaluation of the synovial fluid, bone marrow, and peripheral blood revealed large numbers of abnormal lymphoid cells labeling a 4B4-positive, CD4-positive, IL-2 receptor-negative, helper T cells. Hypergammaglobulinemia, immune complexes, high levels of serum IL-2 receptors, serum antibodies against foreign alloantigens, and specific cytolysis of the patient's leukemic cells by his normal CD8+ T lymphocytes suggest an interaction of the malignant cells and his normal immune cells. Thus, some of the rheumatologic symptoms leading to the diagnosis of leukemia appear to reflect an immunoregulatory imbalance manifested by B-cell hyperactivity, likely induced by the malignant helper T cells, and attempted regulation of his malignant T cells by normal lymphocytes.
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PMID:T helper-cell leukemia/lymphoma: presentation as an acute immune-mediated illness. 213 65

Subsets of lymphocytes infiltrating the gastric mucosa were phenotyped by their surface antigens in biopsies of 30 patients with chronic gastritis (12 with superficial, 9 with atrophic gastritis and 9 with gastric atrophy) and 10 controls. Using direct and indirect immunofluorescent staining, monoclonal antibodies OKT3, OKT4, OKT8, OKB7, antiLeu11b and anti-IL-2 receptor were employed to detect T cell subsets, B cells, NK cells and activated cells. Most of the infiltrating lymphocytes were T cells expressing the CD4 phenotype. B cell proportions were found to increase in relation to the severity of the gastric lesion. IL-2 receptor positive cells were significantly increased in superficial gastritis. These findings indicate an involvement of T cells in the pathogenesis of chronic gastritis. Furthermore, the predominance of CD4 positive cells together with the increase of B cells parallel to the severity of the gastric lesion possibly support the concept of a T-B cooperation leading to tissue damage.
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PMID:Immunohistological phenotyping of the stomach infiltrating lymphocytes in chronic gastritis. 214 68

Thymocyte cell suspensions, prepared from mice at different ages, were cultured in vitro with human rIL-2. This stimulation resulted in a cell population that contained almost 50% TCR-gamma delta-positive cells if thymocytes were taken from fetal day 17 until just after birth. Analysis of the variable (V gamma) region used by the TCR-gamma delta cells revealed that 90% of them expressed TCR-V gamma 3, and less than 5% expressed TCR-V gamma 2. Cells positive for TCR-alpha beta were barely detectable. If fetal day 18 organ cultured thymus lobes, instead of a cell suspension, were stimulated with IL-2, no rise in the number of TCR-V gamma 3+ or TCR-delta+ cells was observed, whereas a partial outgrowth of TCR-alpha beta+ cells occurred. From day 1 after birth, the number of TCR-gamma delta cells recovered from an IL-2-stimulated thymocyte cell suspension dropped to reach a plateau of 15% of the total cell number, whereas TCR-V gamma 3+ cells became undetectable in older animals. TCR-alpha beta+ cells, on the other hand, quickly rose in cell number after birth. Kinetic analysis showed that the preferential outgrowth of TCR-V gamma 3+ cells in IL-2-stimulated fetal day 18 thymocyte cell suspensions was present from the onset of the culture; a significant proliferation of CD4 or CD8 single positive TCR-alpha beta cells was never observed. This lack of proliferation of TCR-alpha beta cells was not due to inhibition by the activated TCR-V gamma 3+ cells. Throughout the IL-2 culture, one-fourth of the TCR-V gamma 3+ thymocytes was positive for CD8. Analysis of the DNA content and the IL-2 receptor (IL-2R) p55 expression showed that during the first days of culture the TCR-V gamma 3+ cells had a much higher proliferation rate than the TCR-V gamma 3- cells, although TCR-V gamma 3+ IL2R p55+ cells could not be detected. From day 3 to 4 of culture, the proliferation rate of TCR-V gamma 3+ cells equaled that of the rest of the cells and less than 20% of the TCR-V gamma 3+ cells expressed the IL-2R p55. The biologic significance of our findings is discussed.
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PMID:Preferential proliferation of T cell receptor V gamma 3-positive cells in IL-2-stimulated fetal thymocytes. 214 32

Tumor infiltrating (TIL) and peripheral blood lymphocytes (PBL) were isolated from 18 patients with non-small cell lung cancer undergoing radical surgery. Surface marker analysis revealed that TILs and PBLs mainly consisted of CD3+ T cells and that TILs generally displayed a lower CD4/CD8 ratio. Differences were found in the expression of CD25 (IL-2 receptor) and DR (MHC class II) antigens, which were increased in TILs, and in the percentage of CD16+ natural killer (NK) cells, which was reduced in TILs as compared to PBLs. Accordingly, the NK activity of TILs was lower than that of PBLs, whereas neither TILs nor PBLs expressed spontaneous cytolytic activity against fresh autologous tumor cells, melanoma cells and the "NK-resistant" A549 lung carcinoma cell line. After 4 days of culture in medium with recombinant-interleukin-2 (rIL-2), TILs and PBLs acquired cytolytic activity against all cell targets, but TILs expressed higher levels of cytotoxicity than autologous PBLs only in 3 patients out of 16 tested. More importantly, both TILs and PBLs displayed similar levels of cytotoxic activity against autologous tumor cells. TILs and PBLs from 8 patients were also analyzed by a limiting dilution microculture system. Cloning efficiency was remarkably lower in TILs, and surface marker analysis of T cell clones confirmed that an accumulation of CD8+ lymphocytes, which displayed cytolytic activity in a lectin-dependent assay, occurred at the tumor site. The non-MHC-restricted cytolytic activity of TIL- and PBL-derived T cell clones against K562, A549, and allogeneic melanoma cells and the cytolytic activity against autologous tumor cells showed no significant differences. Only 53% of TIL clones released IL-2 in response to PHA + TPA stimulation, whereas 68% of PBL-derived clones were IL-2 producers. Moreover, most PBL- and TIL-derived clones released tumor necrosis factor alpha in response to mitogen stimulation.
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PMID:Peripheral blood and tumor infiltrating lymphocytes in non-small cell lung cancer: analysis at the population and clonal level. 217 60

Lymphocyte activation was examined by interleukin-2 (IL-2) receptor expression on peripheral blood mononuclear cells from coeliac and control subjects. Purified T cells were incubated with gluten fraction 111 (a known toxic peptide for coeliac subjects), soyabean hydrolysate (an unrelated hydrolysed food antigen), and Concanavalin-A (Con-A, a non-specific mitogen). After 1-5 days incubation, expression of IL-2 receptors was assessed using a cellular enzyme-linked immunosorbent assay (ELISA). Gluten fraction 111 induced expression of IL-2 receptors on T lymphocytes from coeliac but not from normal subjects (P = 0.0005), whereas soyabean hydrolysate did not induce IL-2 receptor expression. Lymphocytes from both coeliac and normal subjects had similar increased IL-2 receptor expression after incubation with Con-A. Flow cytometry was also used to confirm specific expression of IL-2 receptor expression of lymphocytes from coeliac subjects. Interleukin-2 receptor expression increased from 0 to 5.4% of cultured mononuclear cells after 7 days incubation with gluten fraction III. These cells were CD3-positive and CD4-positive. We conclude that peripheral blood lymphocytes from coeliac subjects are sensitized specifically to gluten fraction III.
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PMID:Lymphocyte activation as measured by interleukin-2 receptor expression to gluten fraction 111 in coeliac disease. 222 30

Total lymphoid irradiation is a radiotherapy procedure used as an alternative immunosuppressive regimen in organ transplantation. Following TLI mature lymphocytes are depleted, and splenocytes do not proliferate to mitogens, produce IL-2, or express IL-2 receptors. We now show that mitogen stimulated splenocytes from TLI-treated mice do not secrete IL-2 protein by an IL-2 ELISA assay. Northern blot analysis and RNase protection assays reveal that TLI splenocytes do not make IL-2 RNA or IL-2 receptor RNA following mitogen stimulation. TLI splenocytes produce at least 1000 times less IL-2 RNA after Con A stimulation than normal splenocytes. TLI therapy resembles anti-CD4 therapy and CsA in that each results in an IL-2-"depleted" state.
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PMID:Mechanisms of total lymphoid irradiation-induced immunosuppression. II. Failure of con A-stimulated splenocytes from TLI-treated mice to express IL-2 and IL-2 receptor RNA. 223 59

Recent studies indicate that intestinal lamina propria T cells are highly specialized lymphocytes, which differ from T cells in other compartments of the immune system in several respects. In the present study phenotypic and functional characteristics of lamina propria T cells and their possible relation to mucosal growth will be discussed. Lymphocytes from human and nonhuman primate intestine were isolated by an enzymatic procedure. Lymphocytes were studied using dual-color immunofluorescence (FACS) and functional in vitro assays. CD4 positive (helper-) lamina propria T-cells lack the CD45RA antigen and express the CD45RO antigen. This phenotype is characteristic for memory T cells. In addition intestinal T cells express IL-2 receptors and IL-2 receptor mRNA, and are able to synthesize high amounts of IL-2. Functional studies in nonhuman primates infected rectally with Chlamydia trachomatis have shown that lamina propria T cells do not proliferate after stimulation with antigen but rather provide helper function for immunoglobulin synthesis. The intestinal lamina propria therefore contains highly specialized T cells which have the phenotype of memory T cells and which are activated. Functionally these T cells can be characterized as differentiated effector lymphocytes. Recent studies from other laboratories have shown that the pattern of lymphokines produced by lamina propria T cells and the responsiveness to certain lymphokines also differ from those of other lymphocyte populations. Since T-cell-derived lymphokines are also important regulators for epithelial growth and differentiation as well as for connective tissue metabolism, lamina propria T cells might be of major importance in mucosal growth and transformation.
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PMID:Special functional features of T-lymphocyte subpopulations in the effector compartment of the intestinal mucosa and their relation to mucosal transformation. 226 60

Envelope glycoprotein gp120 of human immunodeficiency virus type 1 (HIV-1) is known to inhibit T-cell function, but little is known about the mechanisms of this immunosuppression. Pretreatment of a CD4+ tetanus toxoid-specific T-cell clone with soluble gp120 was found to exert a dose-dependent inhibition of soluble antigen-driven or anti-CD3 monoclonal antibody-driven proliferative response, interleukin 2 (IL-2) production, and surface IL-2 receptor (IL-2R) alpha-chain expression, all of which were reversed by the addition of exogenous IL-2. mRNA for the gene encoding IL-2 was suppressed by treatment with gp120, but IL-2R gene transcription was not inhibited. Bypass activation of the T-cell clone with phorbol 12-myristate 13-acetate plus ionomycin was unaffected by gp120 pretreatment. Thus, gp120-CD4 interaction interferes with an essential role of the CD4 molecule in signal transduction through the CD3-antigen receptor (Ti) complex. Such a mechanism of gp120-induced immunosuppression, if operative in vivo, could contribute to the depressed specific immune responses associated with HIV infection.
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PMID:Human immunodeficiency virus type 1 envelope glycoprotein gp120 produces immune defects in CD4+ T lymphocytes by inhibiting interleukin 2 mRNA. 231 27

Monoclonal antibodies to certain cell surface constituents on lymphocytes, monocytes and macrophages have been administered to Lewis rats with developing, established or adoptively transferred arthritis, to determine any immunomodulatory properties. Anti-CD4 antibodies against helper T-lymphocytes produced a dose related inhibition of developing arthritis; high dose levels completely suppressed all symptoms of arthritis and these rats were resistant to further attempts to induce arthritis. Anti-Ia (MHCII) antibodies also inhibited arthritis in a dose related manner; anti-pan T antibodies delayed the onset of arthritis, but antibodies against CD8 and IL-2 receptor positive cells were without effect. Development of type II collagen-induced arthritis was also inhibited by anti-CD4 treatment. Established arthritis could be temporarily inhibited by anti-CD4 antibodies, but rebound of arthritis invariably occurred after stopping treatment, as is the case with cyclosporin A. Similar results with anti-CD4 antibodies were obtained during treatment of arthritis adoptively transferred by arthritogenic T-lymphocytes. From these experiments it is clear that CD4 positive T-lymphocytes have a major role in the induction of adjuvant arthritis and that interaction between CD4 and Ia bearing cells is important. The rebound of arthritis that occurred after withdrawal of anti-CD4 treatment during established disease infers that cells in addition to helper T-lymphocytes are involved in the chronicity of arthritis, but these remain to be elucidated. These findings are discussed in relation to results with monoclonal antibodies in other models of arthritis and human rheumatoid arthritis; the prospects for human therapy are also discussed.
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PMID:Monoclonal antibodies and arthritis. 232 19


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