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 cell surface receptors for PRL and interleukin-2 (IL-2) are structurally distinct, but share regulatory tasks in T lymphocytes. They can stimulate proliferation and activate transcription of over-lapping sets of genes of T cells. PRL and IL-2 receptor activation are both linked to the Jak/Stat (signal transducer and activator of transcription) pathway. We investigated the ability of PRL and IL-2 to activate Stat proteins in different T cell lines. The DNA binding specificities, the reactivities toward Stat-specific antisera, and the mol wt of IL-2- and PRL-induced DNA-binding proteins in Nb2 and C196 T cell lines were investigated. A comparison with the Stat proteins induced by interferon-gamma, PRL, and IL-6 in T47D mammary tumor cells was made. We found that these parameters were indistinguishable for one of the PRL- and IL-2-induced factors. A transcription factor closely related to mammary gland factor-Stat5 is rapidly activated upon interaction of IL-2 and PRL with their respective receptors. Activation of a second protein related to Stat1 was also observed. Our results emphasize the role of PRL as a regulator of the immune response and indicate that the Stat factors mammary gland factor-Stat5 and Stat1 play a role in the regulation of gene expression during T cell development.
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PMID:Prolactin and interleukin-2 receptors in T lymphocytes signal through a MGF-STAT5-like transcription factor. 758 26

In C57BL/6 mice transgenic for a rearranged gene encoding a V beta 5+ beta-chain of the TCR, transgene expression among CD4+ cells decreases with age, such that approximately 40% of CD4+ cells express an endogenous beta-chain gene in 8-mo-old mice. A similar deletion of V beta 5+ cells is observed among CD4+ cells from nontransgenic littermates. V beta 5+ T cells are deleted intrathymically in I-E+Mtv-9+ strains of mice, but this chronic deletion occurs in the lymphoid periphery, in the absence of I-E. We now demonstrate the increased expression of the activation markers CD44 and VLA-4 among CD4+V beta 5+ cells, in the absence of either an increase in size or IL-2 receptor expression. Functional as well as phenotypic differences distinguish CD4+ from CD8+ cells in older V beta 5+ transgenic mice. Relative to their CD8+ counterparts, CD4+V beta 5+ cells are hyporesponsive to plate-bound anti-V beta 5 Abs, and this anergy is partially reversible by the addition of exogenous IL-2. These data suggest the deletion of CD4+V beta 5+ cells is the result of a process that includes their activation, loss of function, and their eventual removal. To investigate the involvement of the principal V beta 5 superantigen Mtv-9 in this chronic deletion, we have derived several lines of V beta 5+I-E-Mtv-9- mice. Transgene expression also declines with age in CD4+ T cells in these mice, clearly demonstrating that the chronic deletion of CD4+V beta 5+ cells does not require Mtv-9. There is considerable variation in the kinetics and efficiency of CD4+V beta 5+ deletion between lines of Mtv-9- transgenic mice that is not from differences in the profiles of endogenous mammary tumor proviruses nor readily explained by environmental differences that influence proviral expression. These results suggest the existence of genetic factors other than mammary tumor proviruses that influence the deletion of CD4+V beta 5+ cells in the absence of I-E.
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PMID:The induction of peripheral tolerance by the chronic activation and deletion of CD4+V beta 5+ cells. 790 16

The objective was to investigate if the presence of the v-Ha-ras oncogene could induce immune changes different to the ones observed in normal mice. Therefore, we decided to use Oncomice, the transgenic mice with an activated v-Ha-ras oncogene under the control of the mouse mammary tumor virus-promoter, and their normal inbred counterparts, FVB mice. Both strains of mice were fed the Lieber-DeCarli liquid diet with ethanol or the isocaloric control diet and were injected daily with cocaine or saline. The percentage and absolute number of T and B lymphocytes in the spleen and thymus were determined. The in vitro production of TNF-alpha (tumor necrosis factor-alpha), IL-2 (interleukin-2) and IFN-gamma (interferon-gamma) by spleen cells, and the levels of serum sIL-2R (soluble IL-2 receptor) were also measured. Oncomice fed the Lieber-DeCarli ethanol diet or receiving either saline or cocaine injections presented a higher tumor incidence than Oncomice receiving the control diet. A reduced total number of thymocytes as well as absolute number of cells in all the subsets was found in Oncomice. Moreover, a decreased percentage of CD8+ cells was also observed in Oncomouse spleens. These features were even more marked in ethanol-treated Oncomice. Higher serum sIL-2R levels were observed in Oncomice, especially in mice treated with ethanol or cocaine. The results suggest that the oncogene product, P21ras, plays an important role in dysregulating the immune system and hence in favoring tumorigenesis.
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PMID:Effect of ethanol and cocaine treatment of the immune system of v-Ha-ras-transgenic mice. 889 4