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Query: UNIPROT:P14784 (IL-2 receptor)
 3,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By using monoclonal antibodies and flow cytometry, the phenotype and activation state [based on presence of interleukin 2 (IL-2) receptors] were determined on the mononuclear cell (MNC) fraction of ovarian carcinoma tissue from 12 patients. Thymidine incorporation response to IL-2 and phytohemagglutinin stimulation was measured in five cases. By FACS analysis, tumor MNCs contained 79% T cells, 11% monocytes/macrophages, 5% B cells, and 5% natural killer cells. Similar findings were noted in the patients' peripheral blood MNC population. The respective T-helper:cytotoxic/suppressor ratios in tumor and blood MNC populations were less than 1 and approximately 2. The percentage of IL-2 receptor-positive cells was low in both populations. The proliferative response of tumor MNCs was lower than that of blood MNCs from patients and from normal volunteers. These results suggest an intratumor immune suppression, perhaps secondary to the absence of a specific responder population or to the presence of suppressor cells or a soluble factor secreted by the tumor that directly suppresses or affects MNC transport into and out of the tumor.
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PMID:Phenotypic and functional characteristics of mononuclear cells in ovarian carcinoma tumors. 278 70

In this study we have characterized apoptotic cell death of autoreactive T cells resulting from their interaction with astrocytes and the modulatory effect of steroid hormones. Time kinetics of T-cell activation by interferon (IFN)-gamma-treated astrocytes from neonatal Lewis rats and by professional antigen presenting cells (APCs) from bulk suspensions of thymus or spleen were performed. [3H]Thymidine incorporation of neuritogenic P2- and encephalitogenic myelin basic protein (MBP)-specific T-cell lines declined after 48 h in culture with astrocytes. A similar suppressive effect was observed when T cells were cocultured with thymic APCs and astrocytes. This effect disappeared when astrocytes were separated by a transwell system. After 72 h of culture with astrocytes a mean of 17.5 +/- 12.4% T cells exhibited morphological signs of apoptosis. Apoptosis was identified by light microscopy, and confirmed by electron microscopy, by in situ tailing reaction and by agarose gel electrophoresis. Glucocorticosteroids and oestrogen specifically enhanced T-cell apoptosis within 8 h (69.8 +/- 23.1% and 69 +/- 17.1%, respectively) when added after 72 h to the astrocyte system, but not at earlier time points of T-cell activation or when thymic APCs were used. Glucocorticoid-mediated T-cell apoptosis was inhibited by the steroid-receptor antagonist RU 486. Pregnenolone, lipocortin-1, indomethacin and transforming growth factor-beta did not induce apoptosis in this system. The steroid effect was not associated with CD28, IL-2 receptor, or transferrin-receptor expression, which were equally upregulated on T cells activated by astrocytes or thymic APC as shown by fluorescence activated cell sorting (FACS) analysis. We conclude that astrocytes as CNS-specific APC may render T cells susceptible for induction of apoptotic cell death. Some steroid hormones can markedly enhance this process in vitro and may augment an additional effect of a systemic corticosteroid response in vivo during recovery from autoimmune encephalomyelitis.
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PMID:Antigen presentation by astrocytes primes rat T lymphocytes for apoptotic cell death. A model for T-cell apoptosis in vivo. 880 Sep 54