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)

In vivo exposure of B6C3F1 mice to the hepatotoxic chlorinated hydrocarbon, CCl4, suppresses T-cell-dependent humoral immune responses to sRBC. In the present studies, separation-crossover-reconstitution experiments with spleen cell subpopulations isolated from vehicle and CCl4-treated mice (500 mg/kg/day for 7 days) indicate that T-cells are the primary immunologic cell-type altered following CCl4 exposure. Despite suppression of T-cell activity, Con A-activated spleen cell supernatants from CCl4-treated mice produced greater amounts of biologically active IL-2 than untreated spleen cells. Furthermore, Con A-induced upregulation of the p55 subunit of the IL-2 receptor was not altered in spleen cells from CCl4-treated mice. The mediator of immune suppression is a serum-borne factor induced 48 hr following a single exposure to CCl4. Sera isolated from mice treated with CCl4 for 7 days (500 mg/kg/day) or 48 hr following a single exposure (1000 mg/kg) were found to possess high concentrations of TGF-beta 1. Direct addition studies demonstrated that T-cell-dependent AFC responses are more sensitive to suppression by TGF-beta 1 than are T-cell-independent responses. Finally, incubation of sera from CCl4-treated mice with TGF-beta 1-neutralizing mAb reversed the immune suppression associated with this serum. These results demonstrate that CCl4-induced immune suppression is at least partially mediated by induction of TGF-beta 1.
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PMID:Carbon tetrachloride suppresses T-cell-dependent immune responses by induction of transforming growth factor-beta 1. 818 39

Cannabidiol (CBD) is a cannabinoid compound derived from Cannabis Sativa that does not possess high affinity for either the CB1 or CB2 cannabinoid receptors. Similar to other cannabinoids, we demonstrated previously that CBD suppressed interleukin-2 (IL-2) production from phorbol ester plus calcium ionophore (PMA/Io)-activated murine splenocytes. Thus, the focus of the present studies was to further characterize the effect of CBD on immune function. CBD also suppressed IL-2 and interferon-gamma (IFN-gamma) mRNA expression, proliferation, and cell surface expression of the IL-2 receptor alpha chain, CD25. While all of these observations support the fact that CBD suppresses T cell function, we now demonstrate that CBD suppressed IL-2 and IFN-gamma production in purified splenic T cells. CBD also suppressed activator protein-1 (AP-1) and nuclear factor of activated T cells (NFAT) transcriptional activity, which are critical regulators of IL-2 and IFN-gamma. Furthermore, CBD suppressed the T cell-dependent anti-sheep red blood cell immunoglobulin M antibody forming cell (anti-sRBC IgM AFC) response. Finally, using splenocytes derived from CB1(-/-)/CB2(-/-) mice, it was determined that suppression of IL-2 and IFN-gamma and suppression of the in vitro anti-sRBC IgM AFC response occurred independently of both CB1 and CB2. However, the magnitude of the immune response to sRBC was significantly depressed in CB1(-/-)/CB2(-/-) mice. Taken together, these data suggest that CBD suppresses T cell function and that CB1 and/or CB2 play a critical role in the magnitude of the in vitro anti-sRBC IgM AFC response.
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PMID:The profile of immune modulation by cannabidiol (CBD) involves deregulation of nuclear factor of activated T cells (NFAT). 1865 54