肿瘤坏死因子-α在脾脏成纤维细胞网状细胞发育中的重要作用。
Essential role of TNF-alpha in development of spleen fibroblastic reticular cells.
作者信息
Zhao Lintao, Chen Junying, Liu Lina, Gao Jianbao, Guo Bo, Zhu Bo
机构信息
Institution of Oncology, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Institution of Oncology, Xinqiao Hospital, Third Military Medical University, Chongqing, China; Department of Immunology, Third Military Medical University, Chongqing, China.
出版信息
Cell Immunol. 2015 Feb;293(2):130-6. doi: 10.1016/j.cellimm.2015.01.006. Epub 2015 Jan 16.
TNF-alpha plays an important role in the development of secondary lymphoid tissues. Earlier studies showed that fibroblastic reticular cells express TNF-alpha receptor, suggesting that TNF-alpha may affect the development of FRCs. To test this, we analyzed the development and function of FRCs in wild-type or TNF-alpha knockout mice. We found that GP38 expression was down-regulated in the spleen of TNF-alpha knockout mice. Chemokines, mainly secreted by GP38(+) FRCs, were also down-regulated. Additionally, we found that absence of TNF-alpha decreased the homing ability to direct T cells to the spleen. However, absence of TNF-alpha did not affect the development of lymph nodes FRCs. These data reveal that TNF-alpha plays an important role in the development of spleen FRCs. Absence of TNF-alpha could cause abnormality of spleen FRCs, thereby weakening the homing ability of T cells to localize to the spleen T cell zone.
肿瘤坏死因子-α（TNF-α）在次级淋巴组织的发育中起重要作用。早期研究表明，成纤维网状细胞表达TNF-α受体，这表明TNF-α可能影响成纤维网状细胞（FRCs）的发育。为了验证这一点，我们分析了野生型或TNF-α基因敲除小鼠中FRCs的发育和功能。我们发现，在TNF-α基因敲除小鼠的脾脏中，GP38表达下调。主要由GP38(+) FRCs分泌的趋化因子也下调。此外，我们发现TNF-α的缺失降低了将T细胞导向脾脏的归巢能力。然而，TNF-α的缺失并不影响淋巴结FRCs的发育。这些数据表明，TNF-α在脾脏FRCs的发育中起重要作用。TNF-α的缺失可能导致脾脏FRCs异常，从而削弱T细胞定位于脾脏T细胞区的归巢能力。
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