Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P14784 (IL-2 receptor)
 3,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The regulation of rat lymphokine-activated killer (LAK) cell generation from their purified precursors using various cytokines was studied. Several important findings emerged from this study. These include: (i) interleukin-2 (IL-2), but not any other cytokine tested, is pivotal for the development of LAK cells; (ii) transforming growth factor beta 1 (TGF-beta) inhibits IL-2-induced LAK cell differentiation, but not proliferation, regardless of the dose of IL-2 used; (iii) interferon-gamma (IFN-alpha) is inhibitory for LAK cell proliferation, but not differentiation; (iv) tumour necrosis factor-alpha (TNF-alpha) or IFN-gamma synergize with a low but not a high concentration of IL-2; (v) TNF-alpha reverses the anti-differentiative activity of TGF-beta 1 in the presence of a high, but not a low, concentration of IL-2; (vi) anti-p55 IL-2 receptor (R) is not inhibitory for LAK cell development but, on the contrary, a low concentration of this antibody synergizes with IL-2; (vii) IL-1 alpha, IL-1 beta, IL-3, IL-4, IL-6, IFN-alpha. TNF-alpha, or TGF-beta 1 do not affect LAK cell function; and (viii) IL-2 may provide two separate signals for LAK precursors: one is proliferative and the other is differentiative.
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PMID:Differential effects of various cytokines on the generation of rat LAK cells from their purified precursors. 211 78

Transforming growth factors beta (TGF-beta) inhibit the growth of a variety of cell types, including lymphocytes. The immunosuppressive effects of TGF-beta have been attributed to the interference of these molecules with the interleukin-2 (IL-2)-driven component of lymphocyte proliferation. In order to elucidate in more detail the effects of TGF-beta on IL-2-induced proliferation, we investigated the effects of porcine transforming growth factor beta 1 and 2 (pTGF-beta 1 and 2) on the IL-2-driven proliferation of a murine IL-2-dependent T-lymphocyte line (CTLL). The results showed that pTGF-beta 1 and 2 decreased 3H-thymidine incorporation in CTLL cells in a dose-dependent fashion (maximum decrease of 75-85%). Combined-time kinetic analysis of the effects of pTGF-beta on 3H-thymidine incorporation, cell growth, and cell-cycle distribution (monitored as DNA content distribution) revealed that, in the first 48 h of culture, pTGF-beta 1 increased the doubling time from 11.4 to 19.2 h without significantly affecting the cell-cycle distribution of CTLL cells. After 96 h of culture in the presence of pTGF-beta 1, cells started to accumulate in G0/G1, although at this time point 30% of the pTGF-beta 1-treated cells were still in S-G2/M. Furthermore, during the first 48 h, neither the expression of the 55 kd chain of the IL-2 receptor (IL-2R) nor the expression of the transferrin receptor (TfR) was affected by TGF-beta. After 72 h of culture in the presence of pTGF-beta 1, the expression of the IL-2R and TfR was decreased. The data suggest that in CTLL cells TGF-beta initially slows the progression of cells in all phases of cell cycle. In addition, the initial TGF-beta-mediated decrease of IL-2-induced 3H-thymidine incorporation and cell proliferation in CTLL cells is not due primarily to downregulation of the IL-2R and/or TfR.
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PMID:Transforming growth factors beta slow down cell-cycle progression in a murine interleukin-2 dependent T-cell line. 278 27

Gamma interferon (IFN-gamma) production from cultured human peripheral blood mononuclear cells was studied during stimulation with Staphylococcus aureus Cowan I or S. aureus Wood. IFN-gamma was specifically produced from CD16+ natural killer (NK) cells under stimulation by S. aureus Cowan I or Wood because these strains (i) induced IFN-gamma production exclusively from CD3-, CD4- CD8-, and CD16+ cells and (ii) induced CD69 and interleukin 2 (IL-2) receptor alpha expression on CD16+ cells without simultaneously augmenting CD71 or IL-2 receptor alpha on T cells. The effects of biological agents on the induction of S. aureus-induced IFN-gamma production paralleled those of S. aureus-induced CD69 expression on CD16+ cells: IL-2, IFN-alpha, and indomethacin augmented the S. aureus-induced IFN-gamma production, whereas IL-4, transforming growth factor beta 1, prostaglandin E2, and dexamethasone inhibited it. However, IFN-alpha was unique in that it did not induce IFN-gamma production from NK cells while it simultaneously augmented CD69 expression on NK cells, suggesting a unique pathway in the activation of NK cells. Thus, we may conclude that S. aureus-induced IFN-gamma production appears to faithfully represent NK cell function within peripheral blood mononuclear cells.
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PMID:Gamma interferon is produced by human natural killer cells but not T cells during Staphylococcus aureus stimulation. 833 41

Studies from our laboratory indicate that n-3 (fish oil, FO) lipids at 10% (w/w) in a nutritionally adequate, semipurified diet, and supplemented with equal levels of antioxidants, extended the life span of lupus-prone (NZB/NZW)F1 (B/W) female mice as compared to n-6 (corn oil, CO) lipids. The early rise of autoimmune disease in CO-fed mice was closely linked to the loss of T-cell function. Both IL-2 production and IL-2 receptor expression were reduced due to the loss of naive T-cells and a rise in memory T-cells. Proliferative response to both mitogens and superantigens (staphylococcal enterotoxins A and B) was higher in FO-fed 6.5-mon-old mice. These changes paralleled decreased PGE2 production by splenic cells from FO-fed mice. Analysis of mRNA expression in different organs revealed differential effects of dietary lipids. In FO-fed mice, transforming growth factor beta 1 (TGF beta 1) expression was decreased in kidneys, but splenic tissues had higher expression of TGF beta mRNA. As TGF beta promotes programmed cell death (PCD), we studied the effects of CO and FO on PCD rates in lymphocytes. Both propidium iodide staining and DNA fragmentation were elevated in lymphocytes of FO-fed mice when compared to CO-fed mice of similar age. Also, increased PCD correlated closely with increased Fas gene expression. Thus, in addition to various other antiinflammatory effects, dietary FO appears to increase PCD and prevent accumulation of self-reactive immune cells in lymphoid organs. Further studies are required to dissect the pro- and antiinflammatory mechanisms associated with dietary n-3 and n-6 lipids in modulating autoimmune disorders or malignancy during aging.
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PMID:Modulation of antioxidant enzymes and programmed cell death by n-3 fatty acids. 872 1