Inhibition of T cell MAPKs (Erk 1/2, p38) with thermal injury is related to down-regulation of Ca2+ signaling

被引:12
作者
Fazal, N [1 ]
Choudhry, MA
Sayeed, MM
机构
[1] Loyola Univ, Stritch Sch Med, Dept Surg, Burn & Shock Trauma Inst, Maywood, IL 60153 USA
[2] Univ Alabama, Surg Res Ctr, Birmingham, AL 35294 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2005年 / 1741卷 / 1-2期
关键词
T cell; immune response; burn; rat; MAPK; Erk; 1/2; p38; calcium; cell signaling;
D O I
10.1016/j.bbadis.2004.10.006
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
We evaluated MAPK (Erk 1/2 and p38) signaling mechanisms of altered T-cell-mediated immune responses in thermal injury condition. Rats were subjected to 30% body surface scald burn, and their mesenteric lymph node (MLN) and Peyer's patch (PP) T cells were purified using nylon wool method. Activation of MAPKs, Erk 1/2 and p38 was assessed in T cells by determining its phosphorylation using immunoblot analysis, intracellular immunostaining and confocal microscopy. The results showed a down-regulation of Erk 1/2 and p38 activation in anti-CD3-stimulated T cells from thermally injured animals, compared to Erk 1/2 and p38 in sham rat T cells. The downregulation of MAPKs in T cells was reversed by treatment of T cells with calcium agonist, ionomycin. These data indicate that attenuated MAPKs (Erk 1/2, p38) activation in thermally injured animals' T cells could result from derangement of Ca(2+) mobilization. This finding suggests that T cell signaling derangements with thermal injury involve an altered cross-talk between Ca(2+) mobilization and MAPK signaling mechanisms. (c) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:113 / 119
页数:7
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