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)

During the last few years, several observations outline that the impaired T lymphocyte proliferative capacity in the elderly is due to a reduced interleukin 2 (IL-2) release. To further investigate the activation process during lectin stimulation, aged peripheral blood mononuclear cells (PBMC) were stimulated with phytohemagglutinin (PHA) and assessed for CD25 (IL-2 receptor) and CD71 (transferrin receptor) expression at different intervals of time. Our results provided evidence for a significant decline of both structure induction, above all in the later phase of culture. Indomethacin (INDO) treatment gave rise to an enhancement of CD71 antigen expression only, while prostaglandin E2 (PGE2) supplementation to culture media further decreased either CD25 or CD71 receptor induction. Interferon (IFN)-alpha and IFN-gamma treatment failed to modulate the frequency of CD25+ and/or CD71+ cells. Finally, the expression of CD71 receptor was increased by deferoxamine supplementation, this suggesting a partial involvement of iron overload in the depressed function. Although further studies are required to evaluate at a molecular level the decreased antigen expression, these findings indicate that several mechanism are involved in the elderly-related decline of T lymphocyte activation structures during lectin stimulation.
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PMID:Modulating effects on CD25 and CD71 antigen expression by lectin-stimulated T lymphocytes in the elderly. 177 Feb 20

Dysfunctional monocytes (M phi), exerting their inhibitory functions via prostaglandin E2 (PGE2), have been implicated in the depression of immune responses following major surgical, accidental, and burn trauma. A randomized prospective study of the PG-synthetase inhibitor indomethacin (Indo) was performed in 43 patients undergoing major surgical procedures, to evaluate its efficacy in correcting postoperative abnormalities of the cell-mediated immune system (CMI) and preventing infectious morbidity and mortality. Patients, following gastrectomy (GX) or reconstruction of the abdominal aorta (AG), in the treated group (PIndo), received 100 mg IV of Indo 6 hours postoperatively and 3 x 50 mg IV Indo over 24 hours on postoperative days (D) 1,2,3,4. The rate of infectious complications was recorded. Parameters of CMI evaluated preoperatively (D0) and on D1,D3,D5,D7 were: Delayed type hypersensitivity (DTH) response to recall antigens, mitogen-induced lymphocyte proliferation (LP), interleukin 2 (IL-2) synthesis, and phenotyping of mononuclear blood leukocytes (PBMC's) with the monoclonal antibodies for CD3+, CD4+, IL-2 receptor (IL-2R)+ and LeuM3+ receptor sites. In contrast to the group of untreated patients (Pc), PIndo did not show a depression of their preoperative DTH responses, and they also showed a lower rate of early opportunistic infections. The in vitro test of CMI revealed that there was a higher LP capacity in PBMC's of PIndo (p less than 0.05); the postoperative profile of IL-2 synthesis was not statistically different between the groups. Indomethacin administration resulted in a considerable alleviation of postoperative monocytosis (p less than 0.05) and in a protective effect on lymphocyte receptor expression of CD3+, CD4+, and IL-2R+ cells. From these data it is concluded that in vivo cyclooxygenase inhibition may be useful to prevent impairment of CMI, a crucial predisposing factor of the high susceptibility to postoperative infection.
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PMID:Immunoprotective effects of cyclooxygenase inhibition in patients with major surgical trauma. 210 39

The suppressive effect of normal rat peritoneal exudate cells (PEC) on concanavalin A (Con-A)-induced lymphocyte proliferation was studied. Partial suppression of proliferation was obtained by adding 3% PEC and complete suppression was observed with 6% PEC. The suppressive effect was mediated by W3/25+ plastic-adherent macrophages, which constitute about 60% of normal PEC. Addition of PEC prior to, simultaneously with, or 24 h after, but not 48 h after, the stimulation of lymphocytes with Con A resulted in suppression. Suppressed cultures produced normal or slightly increased amounts of interleukin 2 (IL-2), but the expression of the IL-2 receptor on lymphocytes was decreased. Pre-exposure of PEC to gamma interferon (IFN-gamma) resulted in decreased suppression, whereas IFN-gamma added simultaneously with the lymphocytes had no effect. Catalase reversed PEC-induced suppression and significant synergistic effects were recorded when combined with IFN-gamma. Even completely suppressed cultures were effectively protected from suppression. Indomethacin and combinations of indomethacin with catalase or IFN-gamma did not result in additional protection from PEC-mediated suppression.
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PMID:Synergistic action of gamma interferon and catalase to reverse the suppressive effect of peritoneal macrophages on concanavalin A-induced lymphocyte proliferation. 308 21

Patients with active Hodgkin's disease (HD) often demonstrate an impaired T-cell proliferative response to phytohemagglutinin (PHA). The present study examined if interleukin regulation of the PHA response was defective in HD. The Hodgkin's PHA response was impaired at all concentrations of PHA utilized. Indomethacin increased the proliferative response but did not bring it to control levels. Stimulation of the cells with both PHA and irradiated Ia+ B cells normalized proliferation despite identical PGE2 concentrations as in the PHA alone cultures. Hodgkin's monocytes produced normal amounts of interleukin 1 (IL-1). Interleukin 2 (IL-2) production by Hodgkin's T cells was decreased in the PHA stimulated cultures, but was normal in the PHA and Ia+ cell stimulated cultures. In response to PHA stimulation alone, Hodgkin's T cells expressed less IL-2 receptor than control cells. The data suggest the diminished PHA response in HD is due to impaired IL-2 production resulting in diminished IL-2 receptor expression. However, when an Ia+ cell source is added to PHA as an additional stimulator, both TCGF production and proliferation are normalized. Monocytes serve to modulate the magnitude of the PHA response through production of both interleukin 1 and PGE2. However, in the presence of sufficient IL-2 production the influence of monocytes is minimized.
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PMID:Impaired interleukin regulation of the phytohemagglutinin response in Hodgkin's disease. 392 53