TNF receptor p55 is required for elimination of inflammatory cells following control of intracellular pathogens.
TNF receptor p55 is required for elimination of inflammatory cells following control of intracellular pathogens.
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DOI：
10.4049/jimmunol.163.7.3883
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发表时间：
1999-10
影响因子：
4.4
通讯作者：
S. Kanaly;M. Nashleanas;B. Hondowicz;P. Scott
中科院分区：
文献类型：
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作者：
S. Kanaly;M. Nashleanas;B. Hondowicz;P. Scott
一旦病原体被清除，炎性病变内淋巴细胞的消除是疾病消退的关键组成部分。我们在这里报告，通过肿瘤坏死因子受体p55（TNFRp 55）的信号需要消除与细胞内病原体相关的病变淋巴细胞。因此，TNFRp 55-/-小鼠，而不是Fas缺陷小鼠，保持与利什曼原虫或马红球菌感染相关的炎性病变，尽管它们产生了Th 1应答并控制了病原体。炎性细胞从L. major或R. equi感染的C57 BL/6小鼠对TNF诱导的凋亡敏感，相反，与野生型小鼠相比，TNFRp 55-/-小鼠病变中的凋亡细胞数量显著减少。此外，在体内消耗野生型小鼠的TNF阻断了R。马传染病两者合计，我们的研究结果表明，通过TNFRp 55，而不是Fas，信号传导是必需的，以诱导T细胞凋亡的炎症病变内，一旦病原体被消除，在它的情况下，病变不能消退。
The elimination of lymphocytes within inflammatory lesions is a critical component in the resolution of disease once pathogens have been cleared. We report here that signaling through the TNF receptor p55 (TNFRp55) is required to eliminate lymphocytes from lesions associated with intracellular pathogens. Thus, TNFRp55-/- mice, but not Fas-deficient mice, maintained inflammatory lesions associated with either Leishmania major or Rhodococcus equi infection, although they developed a Th1 response and controlled the pathogens. Inflammatory cells from either L. major- or R. equi-infected C57BL/6 mice were sensitive to TNF-induced apoptosis, and conversely the number of apoptotic cells in the lesions from TNFRp55-/- mice was dramatically reduced compared with wild-type mice. Furthermore, in vivo depletion of TNF in wild-type mice blocked lesion regression following R. equi infection. Taken together, our results suggest that signaling through the TNFRp55, but not Fas, is required to induce apoptosis of T cells within inflammatory lesions once pathogens are eliminated, and that in its absence lesions fail to regress.