Heligmosomoides polygyrus induces TLR4 on murine mucosal T cells that produce TGFbeta after lipopolysaccharide stimulation.
Heligmosomoides polygyrus induces TLR4 on murine mucosal T cells that produce TGFbeta after lipopolysaccharide stimulation.
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发表时间：
2006
影响因子：
4.4
通讯作者：
M. N. Ince;D. Elliott;Tommy Setiawan;A. Blum;A. Metwali;Ying Wang;J. Urban;J. Weinstock
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文献类型：
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作者：
M. N. Ince;D. Elliott;Tommy Setiawan;A. Blum;A. Metwali;Ying Wang;J. Urban;J. Weinstock
蠕虫是免疫调节剂，下调炎症性肠病中的结肠炎。在动物模型中，肠道细菌驱动结肠炎，在人类中，LPS受体蛋白TLR 4的某些等位基因增加炎症性肠病的易感性。为了了解肠道蠕虫的免疫调节，我们研究了肠道Heligmosomoides polygyrus定植对LPS诱导的小鼠固有层单核细胞（LPMC）细胞因子反应的影响。LPS不刺激未感染小鼠LPMC产生TGF β。LPS强烈诱导蠕虫感染动物的LPMC分泌TGF β，但不分泌TNF-α或IL-12。TGF β来源于粘膜T细胞。蠕虫感染上调TLR 4表达仅在固有层T细胞。来自蠕虫感染的TLR 4突变体动物的LPMC对LPS没有反应，表明LPS需要TLR 4来刺激TGF β分泌。因此，在蠕虫感染期间，LPS刺激诱导粘膜T细胞通过TLR 4依赖性过程产生TGF β，而不促进促炎细胞因子的合成。
Helminths are immune modulators that down-regulate colitis in inflammatory bowel disease. In animal models, intestinal bacteria drive colitis and in humans certain alleles of the LPS receptor protein TLR4 increase inflammatory bowel disease susceptibility. To understand helminthic immune modulation in the gut, we studied the influence of intestinal Heligmosomoides polygyrus colonization on LPS-induced lamina propria mononuclear cell (LPMC) cytokine responses in mice. LPS did not stimulate TGFbeta production from LPMC of uninfected mice. LPS strongly induced LPMC from worm-infected animals to secrete TGFbeta, but not TNF-alpha or IL-12. The TGFbeta derived from mucosal T cells. Helminth infection up-regulated TLR4 expression only in lamina propria T cells. LPMC from worm-infected TLR4 mutant animals did not respond to LPS, suggesting that LPS required TLR4 to stimulate TGFbeta secretion. Thus, during helminth infection, LPS challenge induces mucosal T cells to make TGFbeta through a TLR4-dependent process without promoting synthesis of proinflammatory cytokines.