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)

The incidence of activation markers on proliferating CD4+, CD4+ CD8+ and CD8+ lymphocyte subsets was determined in a single laser Epics-C fluorescence-activated cell sorter system, using a series of double staining combinations. Experiments were performed after 3 days of culture with PHA on cell fractions enriched for CD4+ or CD8+ lymphocytes before initiation of culture. The percentage of CD4+, CD4+ CD8+ and CD8+ lymphocytes in the total population was determined using double staining with Leu3 PE for the detection of CD4+ cells, and Leu2 FITC for the detection of CD8+ cells. Next, double stainings with Leu3 and Leu2 antibodies conjugated with PE and antibodies directed against activation markers (M) IL-2 receptor, transferrin receptor, HLA-DR antigen and CALLA conjugated with FITC were performed, using the following combinations: Leu3 and Leu2/M, Leu3/M and Leu2/M. The expression of activation markers on CD4+ CD8+ lymphocytes was calculated from the results. Our findings indicate that CALLA is expressed on most CD4+ and all CD4+ CD8+ cells, and on a small percentage of CD8+ lymphocytes; the IL-2 receptor was expressed on most CD4+ cells, on approximately three-quarters of CD4+ CD8+ cells and half the CD8+ cells; HLA-DR was expressed on a small percentage of CD4+ cells, all CD4+ CD8+ cells and half of CD8+ cells. The transferrin receptor was almost exclusively expressed on CD4+ CD8+ cells. The standard deviation of the calculated values did not exceed 13% and this analysis can generally be applied to determine the co-expression of a third marker in a mixture of single and double stained cells using conventional methods.
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PMID:Determination of co-expression of activation antigens on proliferating CD4+, CD4+ CD8+ and CD8+ lymphocyte subsets by dual parameter flow cytometry. 295 Jan 75

Propranolol (PRO) is a beta-adrenergic receptor antagonist. The studies were aimed to evaluate the effect of a single intravenous PRO injection at a dose of 0.1 mg/kg on some immune parameters, and were performed on 12 men, including 9 duodenal ulcer patients and 3 healthy subjects, aged 19-23 years (mean 20.5 +/- 1.2). Blood samples were drawn before, 30 and 150 min following the injection. Results obtained in duodenal ulcer patients and healthy subjects revealed the same type of changes. A single PRO injection did not significantly affect total peripheral blood lymphocyte, Th cell and monocyte counts; however, it slightly but significantly lowered numbers of T and Ts cells, which was accompanied by a rise in Th/Ts cell number ratio and NK cell numbers. PRO significantly augmented spontaneous as well as PHA-stimulated IL-2 receptor expression, IL-2 generation, NK cell activity and AMLR observed at 30 and 150 min after the drug injection. Possible mechanisms of these changes are discussed.
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PMID:The stimulatory effect of a single intravenous dose of propranolol of some immune parameters in humans. 296 80

Alteration of T cell surface marker expression with a decrease of CD3 positive cells relative to the number of CD4 and CD8 positive cells, diminished in vitro proliferative response to mitogenic stimuli like PHA and antibodies to the CD3/Ti complex, and increase in serum IL-2 receptor levels, are among the changes in immunologic parameters that have been associated with advanced age. To distinguish between effects of the primary aging process and diseases of aging not known to be directly related to immune function, we investigated these variables in two well characterized populations of elderly donors (greater than 70 years) and a young adult control group (less than 35 years). The first group of older donors reported no evidence of significant chronic or recent acute illness and saw a physician only for routine medical care. The second group was randomly selected from individuals seen in a geriatric medicine clinic for diagnoses that included osteoarthritis and cardiopulmonary disorders. Altered surface marker expression and increased serum IL-2 receptor levels were seen only in the second group. On the other hand, lymphocyte proliferative responses to PHA, Leu 4 (anti-CD3) and a monoclonal antibody to the beta-chain of the T cell antigen receptor (WT31) were significantly decreased in both populations. Because we would expect primary aging to affect even extremely fit individuals of advanced age, we conclude that decrease in T cell proliferative response may represent a biomarker of primary aging in man. The alteration in surface marker expression and increased IL-2R levels in serum appear to be effects secondary to non-immunologic disease rather than aging.
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PMID:Lymphocyte proliferative response to PHA and anti-CD3/Ti monoclonal antibodies, T cell surface marker expression, and serum IL-2 receptor levels as biomarkers of age and health. 296 40

We studied the expression of the interleukin-2 (IL-2) receptor and the proliferative response to exogenous IL-2 of peripheral blood leukemic cells from patients with adult T cell leukemia (ATL) in order to see whether IL-2 receptor expressed on ATL cells is different from normal IL-2 receptor and whether it plays a role in the neoplastic growth in ATL. Peripheral blood leukemic cells from 42 patients with ATL examined expressed IL-2 receptors that were detected by anti-Tac monoclonal antibody when examined immediately after the separation of cells or after the culture for 24 or 48 h. The number of anti-Tac binding sites ranged from 3,100 to 11,400 in fresh cells and from 3,600 to 96,000/cell in short-term cultured leukemic cells, whereas phytohemagglutinin-P (PHA-P)-stimulated normal T cells exhibited 6,900-35,000 anti-Tac binding sites per cell. ATL-derived and human T cell leukemia/lymphoma virus, type I (HTLV-I)-infected cell lines such as MT-1 and Hut102 expressed a much higher number of anti-Tac binding sites. Leukemic cells from 15 patients with ATL examined showed no or very poor proliferative response to various concentrations of immunoaffinity-purified IL-2, although they expressed Tac antigen (Ag). Radiolabeled IL-2 binding experiments demonstrated that ATL leukemic cells could bind IL-2, and they expressed both high and low affinity IL-2 receptors, although the number of high affinity IL-2 receptor was much less than that of low affinity IL-2 receptor and that of anti-Tac binding sites. In contrast, leukemic T cells from a patient with T cell chronic lymphocytic leukemia (CLL), in whom HTLV-I infection was not demonstrated, responded as well as PHA-P-stimulated normal T cells, and their IL-2 receptors, unlike ATL cells, were modulated (down regulated) by anti-Tac antibody. No differences were noted between ATL cells and normal activated T cells in one-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis analysis of the IL-2 receptor. Thus, leukemic cells in ATL spontaneously and continuously express IL-2 receptor, which appears to be abnormally regulated and unresponsive to IL-2. These results, taken together with those on normal IL-2 receptors on HTLV-I-negative T-CLL cells, suggest that abnormal expression of the IL-2 receptor in ATL is closely associated with HTLV-I infection and may play a role in the neoplastic growth of ATL cells.
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PMID:Interleukin-2 receptor (Tac antigen) expressed on adult T cell leukemia cells. 299 59

Peripheral lymphocytes stimulated with phytohemagglutinin (PHA-blasts) were examined for their responsiveness to exogenous interleukin 2 (IL-2). The proliferative response of PHA-blasts to IL-2 was significantly lower in patients with systemic lupus erythematosus (SLE) than in normal subjects. To clarify the reason for this defect, the expression of IL-2 receptor (IL-2R) on PHA-blasts was investigated using anti-Tac antibody and purified IL-2. Cytofluorometric analysis showed no statistical differences in the Tac positivity of PHA-blasts among normal subjects and patients with active and inactive SLE. Scatchard analysis using 125I-labeled anti-Tac monoclonal antibody revealed that the number of Tac epitopes on PHA-blasts was also not different among them. Next, the affinity of IL-2R expressed on PHA-blasts was determined by Scatchard analysis using radiolabeled IL-2 as a ligand. The number of high affinity IL-2R on the PHA-blasts was significantly decreased in patients with active and inactive SLE, as compared with normal subjects. The responsiveness of PHA-blasts to exogenous IL-2 was well correlated to the number of high affinity IL-2R, but not to the number of Tac epitopes or total IL-2R. Inasmuch as high affinity components of IL-2R are functionally active, the defective expression of high affinity IL-2R may be responsible for the T cell dysfunctions in SLE.
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PMID:Impaired expression of high affinity interleukin 2 receptor on activated lymphocytes from patients with systemic lupus erythematosus. 311 22

The uptake of free calcium ion (Ca2+) in PHA- or A23187-stimulated lymphocytes was measured using 45CaCl2 and 3H-water. Augmentation of Ca2+ uptake by both mitogens was observed, but the enhanced uptake occurred transiently, sometime within 30 min of the stimulation. The total amount of calcium in quiescent lymphocytes as determined by atomic absorption spectroscopy was about 2.9 X 10(-15) g/cell. When stimulated with PHA, more calcium gradually accumulated in the cells. The maximum amount of accumulation occurred at around 40 h, and was about 2-fold higher than that of control cells. In A23187-stimulated cells, the calcium content increased within 1 h by about 4-fold, reached a maximum at about 6 h (6-fold) and thereafter, surplus calcium was pumped out. The cytosolic free calcium ion concentration (the [Ca2+]i) within single cells was measured using quin 2 or fura-2. The [Ca2+]i was about 1 X 10(-7) M, and a transient increase in the [Ca2+]i was observed in some cells within 1 min after Con A-stimulation. Another rise in the [Ca2+]i was observed around the 40th h, and the maximum expression of the IL-2 receptor was observed at about this time. Therefore the results may indicate that the IL-2-mediated lymphocyte transformation is dependent on the rise in the [Ca2+]i.
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PMID:Calcium ion influx during mitogenic stimulation of lymphocytes. 311 49

PHA activated human peripheral blood mononuclear cells (MNC) were incubated with human interleukin 2 (IL-2) in the absence or in the presence of 10(-6)-10(-9) M hydrocortisone (HC). HC suppressed the proliferative response of the activated MNC to highly purified human leucocyte IL-2 in a dose dependent manner. This suppression was in full accordance with an inhibition of the IL-2 binding capacity, whereby the high affinity binding sites were reduced by 85%, while the low affinity sites were less affected. The mechanism by which HC inhibits the binding of IL-2 is still unknown. Evidence is presented that HC binds only weakly to IL-2. We conclude that HC interferes with the IL-2 binding by modulating the binding and/or signal processing function of the IL-2 receptor.
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PMID:Corticosteroid-interleukin 2 interactions: inhibition of binding of interleukin 2 to interleukin 2 receptors. 311 40

The aim of this study was to examine the effect in vitro of gold sodium thiomalate (GST) on interleukin 1 (IL-1), and interleukin 2 (IL-2) production and IL-2 receptor expression in thymocytes of mice and in human peripheral blood mononuclear cells (PBMC). GST increased the proliferation of thymocytes and PBMC to suboptimal doses of T cell mitogens Con A and PHA. It induced IL-1 production of the accessory adherent cells within thymocytes and PBMC, IL-1 production in the murine macrophage line P388D1 and induced the PHA reactive thymocytes to produce IL-2 and to express IL-2 receptors. The significance of these findings is discussed.
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PMID:In vitro effects of gold sodium thiomalate on IL-1, IL-2 production, IL-2 receptor expression and IL-2 responsiveness in thymocytes and peripheral blood mononuclear cells. 311 45

Peripheral blood mononuclear cells from young adult and aged human donors were activated with PHA and the expression of IL-2 receptors was examined. For the detection of IL-2 receptor-positive cells, flow cytofluorometry using monoclonal antibody Clonab IL-2R, fluorescein-conjugated swine anti-mouse IgG and fluorescence activated cell sorter FACS 440 were utilized. The age-related decrease in the expression of IL-2 receptors was observed: the percentage of IL-2 receptor-positive PBMC was substantially higher in the group of young adult donors than in the group of the aged individuals.
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PMID:Expression of IL-2 receptors on peripheral blood lymphocytes from young adult and aged human donors. 311

Cellular and genetic analyses of interleukin-2 (IL-2) production and IL-2 receptor (IL-2R) expression were examined in a immunodeficient patient and his family members. Mononuclear cells (MNC) of the patient showed no proliferative response (stimulation index, less than 2) to T-cell mitogens (PHA and Con A) and were defective in IL-2 production and IL-2R expression (less than 1%), whereas productions of other lymphokines (B-cell differentiation factor and IFN-gamma) were not impaired significantly. His brother died of the same disease and his father also lacked in proliferative response and IL-2 production by PHA stimulation. In Southern blot analyses using DNA probes of IL-2 and IL-2R, patterns of the patient were the same as those of healthy volunteers, whereas the transcription of DNA coding for IL-2R to mRNA was lacking in the patient. These results suggest that inheritant defects of IL-2 production and IL-2R expression reside in this family and the defects are not linked to DNAs coding for IL-2 and IL-2R but to a transcriptional deficiency.
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PMID:Cellular and genetic analyses of IL-2 production and IL-2 receptor expression in a patient with familial T-cell-dominant immunodeficiency. 312 Dec 26


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