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)

A T-cell replacing factor (TRF)/interleukin-5 (IL-5) is a B-cell growth and differentiation factor. In the present study, we examined the role of TRF/IL-5 in the increase in the levels of interleukin-2 (IL-2) receptor expression on activated B-cells. High pressure liquid chromatography (HPLC)-purified TRF/IL-5 (B151-TRF) from TRF-producing T-cell hybridoma, B151K12, as well as recombinant TRF/IL-5 (rec-TRF) were used for the analysis. Maximum anti-2,4-dinitrophenyl (DNP) IgG antibody response of DNP-primed B-cells or polyclonal IgM secretion of B-cell tumor line BCL1 was seen when HPLC-purified B151-TRF was added or when suboptimal doses of B151-TRF were added to the culture in the presence of IL-2. Normal resting B-cells gave maximum anti-SRBC IgM PFC responses when HPLC-purified B151-TRF and IL-2 were present. The purified B151-TRF as well as rec-TRF also induced on B-cells increased expression of IL-2 receptors that react with monoclonal anti-murine IL-2 receptor antibody, PC61, and 125I-labelled IL-2. The numbers of functional high affinity IL-2 receptors on activated B cells increased at least 20-fold by culturing them with purified B151-TRF. Moreover, B151-TRF induced increase in the levels of steady-state mRNA for IL-2 receptor by approximately 8-fold. These results suggest that activated B-cells as well as BCL1-cells may express functional IL-2 receptors or closely related molecules when stimulated with HPLC-purified B151-TRF as well as rec-TRF.
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PMID:T cell replacing factor/interleukin 5 induces not only B-cell growth and differentiation, but also increased expression of interleukin 2 receptor on activated B-cells. 311 78

The B-cell differentiation-inducing activity of interleukin-1 (IL-1) was compared with that of T-cell replacing factor (TRF)/interleukin-5 (IL-5), which was originally described as a late-acting B-cell differentiation-inducing factor. Human recombinant IL-1 and murine recombinant TRF/IL-5 were used in this study. Purified B cells from non-primed or antigen-primed mice, LPS-stimulated B-cell blasts, and chronic B-cell leukaemia (BCL1) cells were used as the responding B-cell population. Addition of IL-1 to the culture of normal B-cells and sheep red blood cells (SRBC) induced a dose-dependent anti-SRBC IgM response, with maximal response at 100 U/ml, whereas the response induced by TRF/IL-5 was less than that induced by IL-1 and did not reach the maximum even at 100 U/ml. Addition of anti-IL-1 antibody, but not anti-TRF/IL-5 antibody or anti-IL-2 receptor antibody, inhibited IL-1-induced anti-SRBC responses. Depletion of cells adherent to Sephadex beads from splenic B cells showed no significant effect on the magnitude of the total responses. IL-1 could induce little, if any, differentiation in antigen-primed B cells, LPS-stimulated B-cell blasts, or BCL1 cells into antibody-secreting cells, whereas differentiation could be induced by low doses of TRF/IL-5 (1-2 U/ml). Of great interest is that suboptimal doses of IL-1 (10 U/ml) could synergize with TRF in the primary anti-SRBC PFC responses. Kinetic studies revealed that IL-1 acts on B cells for the first 2 days and TRF/IL-5 for the last 3 days in 5-day cultures of B cells. These results suggest that IL-1 acts primarily on resting B cells as a differentiation-inducing factor in the presence of antigen, and also acts as a 'priming' factor for TRF/IL-5.
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PMID:Role of recombinant interleukin-1 compared to recombinant T-cell replacing factor/interleukin-5 in B-cell differentiation. 328 Apr 72

Primary biliary cirrhosis (PBC) is a chronic cholestatic autoimmune liver disease characterized by selective destruction of the intrahepatic bile ducts and highly specific serum anti-mitochondrial autoantibodies (AMA). Several studies have attempted to determine the cytokine pattern characterizing PBC, yet no definitive data have been gathered. The present study was designed to evaluate pro-inflammatory cytokines (IL-1beta, IL-6, TNFalpha), soluble IL-2 receptor (sIL-2R, e.g. soluble CD25), and complement components (C1q, C3, factor B, properdin) levels in sera from 84 patients with PBC and 41 controls. PBC was characterized by significantly higher levels of all pro-inflammatory cytokines when compared to controls; these included IL-1beta (433.3 +/- 13.2 vs. 316.6 +/- 14.7 pg/ml, P < 0.001), IL-6 (701 +/- 17.4 vs. 158 +/- 22.5 pg/ml, P < 0.001), TNFalpha (3.38 +/- 0.6 pg/ml vs. undetectable, P = 0.001), and sIL-2R (1527.1 +/- 106 vs. 566.4 +/- 28.7 U/ml, P < 0.001). Similarly, all complement components were also significantly higher in PBC compared to control sera. In conclusion, PBC sera manifest higher levels of sIL-2R and complement components and this may reflect a perpetuated immune activation. As expected, we also report that all major pro-inflammatory cytokine levels are enhanced in PBC. Further longitudinal analyses could demonstrate a correlation between these markers and disease stage or inflammatory activity, to predict histological staging, disease activity, and response to treatment.
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PMID:Serum inflammatory cytokines, complement components, and soluble interleukin 2 receptor in primary biliary cirrhosis. 1984 77