期刊
SHOCK
卷 18, 期 3, 页码 212-216出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00024382-200209000-00002
关键词
T lymphocyte; spleen; src-kinases; P59(fyn); nuclear factors; IL-2; Con A; indomethacin; rat
资金
- NIAAA NIH HHS [R21AA12901-01A1] Funding Source: Medline
- NIGMS NIH HHS [R01 GM53235, R01 GM56865] Funding Source: Medline
PGE2 is known to suppress T cell proliferation and IL-2 production in many inflammatory conditions. Previous studies from our laboratory have shown that such suppression of T cell proliferation in burn and sepsis could result from alteration in T cell activation signaling molecule p59(fyn). In this study, we examined the role of downstream signaling molecules NFAT and AP-1 in PGE(2)-mediated suppression of T cell in burn injury. These studies were carried out utilizing splenic T cells from sham and burn rats 3 days after injury. The data presented in this manuscript suggest a significant suppression of IL-2 production by T cells from burn injured rats compared with the T cells from sham rats. The suppression in T cell IL-2 production was accompanied by a decrease in the activation of NFAT and AP-1 as well as a decrease in T cell p59(fyn) kinase activity. The treatments of burn-injured animals with PGE2 synthesis blocker indomethacin prevented both the decrease in NFAT and AP-1 binding to IL-2 sequences. In vitro incubation of control rat T cells with PGE2 suppressed the activation of NFAT and AP-1. These results suggested that the suppression of T cell IL-2 production could result from PGE2-mediated alterations in the T cell signaling molecule p59(fyn) and NFAT/AP-1.
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