CD90(+)CD45(−) intraperitoneal mesothelial-like cells inhibit T cell activation by production of arginase I

•Intraperitoneal CD90(+)CD45(−) cells grow with mesothelial morphology in culture.•The cells highly express arginase I and strongly inhibit T cell activation.•The cells downregulate CD3 ζ chain expression on activated T cells.•CD3 ζ chain is reduced in intraperitoneal T cells than in circulating T c...

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Veröffentlicht in:Cellular immunology 2014-03, Vol.288 (1-2), p.8-14
Hauptverfasser: Kitayama, Joji, Emoto, Shigenobu, Yamaguchi, Hironori, Ishigami, Hironori, Yamashita, Hiroharu, Seto, Yasuyuki, Matsuzaki, Keisuke, Watanabe, Toshiaki
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Sprache:eng
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Zusammenfassung:•Intraperitoneal CD90(+)CD45(−) cells grow with mesothelial morphology in culture.•The cells highly express arginase I and strongly inhibit T cell activation.•The cells downregulate CD3 ζ chain expression on activated T cells.•CD3 ζ chain is reduced in intraperitoneal T cells than in circulating T cells.•The CD90(+)CD45(−) cells may negatively regulate intraperitoneal immunity. In this study, we analyzed intraperitoneal cells recovered from human samples and found that CD90(+)CD45(−) cells exist as a minor population but vigorously grow in culture, showing the morphological features of mesothelial cells (MC). Interestingly, the MC highly expressed arginase I and markedly suppressed T cell proliferation with the reduction of CD3 ζ chain expression in T cells stimulated by coated anti-CD3 mAb. The addition of nor-NOHA (500μM), or l-arginine (1mM) mostly restored the inhibitory effect of MC on T cell proliferation as well as the reduced expression of CD3 ζ chain. The expression level of CD3 ζ chain in T cells in the peritoneal cavity was significantly down-regulated from circulating T cells. These results suggest that intraperitoneal free MC have immunomodulatory functions through the control of l-arginine level, and thus may play significant roles in the pathogenesis of various diseases in the peritoneal cavity.
ISSN:0008-8749
1090-2163
DOI:10.1016/j.cellimm.2014.01.008