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)

It has recently been demonstrated that IL-4 inhibits IL-2 receptor expression on T cells. Studies have also shown that IL-4 can inhibit IL-2-induced natural killer cell (NK) cytotoxicity, and that IL-4 in combination with IL-2 and large granular lymphocyte (NK/LGL) cells suppresses Ig synthesis. Therefore, we examine whether IL-2 receptor expression on NK/LGL cells is affected with or without IL-4, using fluorescent receptor analysis. Our results demonstrate that IL-4 inhibits/down-regulates the expression of IL-2 receptors on either phytohemagglutinin or IL-2-stimulated NK/LGL cells.
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PMID:Down-regulation of interleukin-2 receptor expression on natural killer cells/large granular lymphocytes by interleukin-4. 157 Oct 94

A previously described patient with X-linked agammaglobulinemia and growth hormone deficiency developed an echovirus-associated meningoencephalitis and dermatomyositis-like syndrome while being treated with intramuscular gamma globulin and human growth hormone. Initiation of high-dose intravenous gamma globulin resulted in resolution of the clinical symptoms and the patient has remained asymptomatic over the past 55 months. Lymphocyte phenotype analysis at the time of presentation with echovirus infection revealed an increase in CD2+, CD16+, HNK-1+ lymphocytes, a decrease in CD4+ T cells as well as absence of B cells. This elevation in the LGL/NK phenotype resolved with clinical improvement. In addition, there was evidence of lymphocyte activation following the development of echovirus infection (increase in HLA-DR expression and elevated serum IL-2 receptor levels) which resolved with clinical improvement. A muscle biopsy obtained during the period of the dermatomyositis-like syndrome demonstrated a CD8+ lymphocytic infiltrate very similar to the observations in classical dermatomyositis. Taken together, these findings suggest that growth hormone therapy in this patient failed to alter the humoral immunodeficiency. In addition, serum IL-2 receptor levels and lymphocyte phenotyping may be useful adjuncts for monitoring echovirus disease in immunodeficient patients.
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PMID:Lymphocyte analysis in a patient with X-linked agammaglobulinemia and isolated growth hormone deficiency after development of echovirus dermatomyositis and meningoencephalitis. 275 12

Seven independent cell lines were derived from the fusion of migratory cells recovered from explant cultures of metrial glands to SP 2/0, a non-Ig secreting B cell myeloma. The migrating cells came from a pool of metrial glands from day 6-8 pregnant random bred CD1 mice and were assumed to be cells early in the differentiation pathway to granulated metrial gland (GMG) cells. The fused cells were cloned twice at the limiting dilution. Hybridization was confirmed by quantitation of cellular DNA using propidium iodide staining and by karyotyping. Electron microscopy revealed that each of the hybrid cell lines was composed of cells which were lymphoid in appearance, but lacked the granules found in mature GMG cells. The surface phenotype of all lines is CD45+, LGL-1-, asialo GM-1-, IgG-, IgM-, CD3- and CD25- (p55 of IL-2 receptor). Although the hybridomas lack those phenotypic markers which were used to show that GMG cells are related to the natural killer (NK) cell lineage (ie LGL-1, asialo GM-1), they do express the pan-leukocyte marker CD45 as well as the lytic protein, perforin, at levels intermediate to those of SP 2/0 cells and GMG cells. In addition, the hybridomas were observed to preferentially bind the NK target cell YAC and to be capable of lytic activity at temperatures below 30 degrees C. Because these hybridomas may represent fusion to an early progenitor cell of the NK/GMG cell lineage, their continued characterization is of merit.
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PMID:Preliminary characterization of lymphoid hybridoma cell lines derived from the pregnant mouse uterus. 780 68

Interleukin-15 (IL-15) is produced by human bone marrow (BM) stromal cells and can induce CD34(+) hematopoietic progenitor cells (HPCs) to differentiate into CD56(+)CD3(-) natural killer (NK) cells in the absence of stromal cells. IL-15 mediates its effects by signaling through the beta and gammac chains of the IL-2/15 receptor (R). The c-kit ligand (KL), also produced by stromal cells, enhances the expansion of NK cells from CD34(+) HPCs in the presence of IL-15, but alone has no ability to differentiate NK cells. Mice deficient in KL do not appear to have a quantitative deficiency in NK cells, suggesting that other stromal cell factors may contribute to NK cell expansion. Flt3 ligand (FL) is also produced by BM stromal cells and has homology with KL. Furthermore, mice with a targeted disruption of the FL gene have reduced numbers of NK cells. We evaluated here the effects of FL on human NK cell development and expansion from CD34(+) HPCs. Like KL, FL significantly enhanced the expansion of NK cells from CD34(+) HPCs in the presence of IL-15, compared with IL-15 alone. However, FL alone had no effect on NK cell differentiation. We therefore explored the mechanism by which FL promotes IL-15-mediated NK cell development. FL was found to induce IL-2/15Rbeta (CD122) expression on CD34(bright) HPCs. The CD34(bright) CD122(+) cell coexpressed CD38, but lacked expression of CD7, CD56, NK cell receptors (NKRs), or cytotoxic activity in the absence of IL-15. Using limiting dilution analysis in the presence of IL-15 alone, we demonstrated that the FL-induced CD34(bright)CD122(+) HPCs had an NK cell precursor frequency 20- to 60-fold higher than the CD34(dim/neg)CD122(-) HPCs and 65- to 235-fold higher than fresh CD34(+) HPCs. KL had similar effects as FL, but induced a significantly lower percentage of CD34(bright)CD122(+) cells (P </=.01). Both FL and KL also increased IL-15R transcript in CD34(+) HPCs. Culture of CD34(+) HPCs in FL or KL, followed by culture in IL-15 alone, induced expression of both C-type lectin and Ig-superfamily NKRs on CD56(+) cells. These data collectively support a role for FL in early human NK cell development. FL or KL generate a unique CD34(bright) CD122(+)CD38(+) human NK cell intermediate from CD34(+) HPCs that lacks NK features yet is IL-15-responsive. IL-15 is then required for the induction of CD56 and NKRs, LGL morphology, cytotoxic activity, and the ability to produce abundant cytokines and chemokines.
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PMID:Flt3 ligand promotes the generation of a distinct CD34(+) human natural killer cell progenitor that responds to interleukin-15. 980 58