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 antirejection eicosanoids--PGE2, (PGD2), and PGI2--have an attenuating effect on T-cell proliferation by inhibition of IL-1, IL-2, and class II antigen expression on macrophages, and the prorejection eicosanoids--TXA2, LTB4, LTC4, and LTD4--enhance T-cell proliferation. LTB4 stimulates IL-1 and IL-2 formation and expression of IL-2 receptor. The mechanism of enhancement of T-cell proliferation by TXA2 has not been demonstrated. LTC4 and LTD4 promote gamma-interferon release and can replace IL-2 as a stimulator of gamma-interferon. PAF at high concentrations inhibits lymphocyte proliferation. The eicosanoids interfere with the same mechanisms as CsA and corticosteroids on T-cell clonal expansion. In experimental organ transplantation, corticosteroids can be replaced by compounds preventing the formation or expression of the prorejection eicosanoids or analogs of antirejection eicosanoids as well as by PAF antagonists. In addition, these drugs exert synergistic effect with CsA and azathioprine.
Adv Prostaglandin Thromboxane Leukot Res 1987
PMID:Leukotrienes, thromboxane, and platelet activating factor in organ transplantation. 295 38

Undoubtedly, synovitis is a cell-mediated process involving various cell types, such as T cells, B cells, APC, monocytes/macrophages, synoviocytes, chondrocytes, and cytokines. Therefore, it is difficult to clarify the cell type that plays the central role in the inflammatory process. Despite this difficulty, there is strong evidence that T cells mediate the disease in collaboration with APC that bear specific antigenic peptides. The mediators released could perpetuate an ongoing inflammatory process in the joints irrespective of the nature of the initiating agents. Therefore, many approaches to a more specific immunotherapy for RA have been developed, directed toward the modulation of T cell function. Thus far, various forms of chemical and biologic treatment have been used, such as cyclosporin A and monoclonal antibodies directed against T-cell epitopes and IL-2 receptor, with some beneficial effects on the course of RA. The development of a more specific immunotherapy using reagents directed against the T-cell receptor and vaccination with specific T cells await further studies, since we still do not know the inciting antigen(s) in RA. Nevertheless, we are hopeful that the ongoing search for the still unknown antigen(s) will be successful, thus providing new and better treatment regimens for a still uncurable disease.
Adv Prostaglandin Thromboxane Leukot Res 1994
PMID:Basic mechanisms in rheumatoid arthritis: the role of T lymphocytes in rheumatoid synovitis. 777 43