NK T cells stimulated with a ligand for TLR2 at least partly contribute to liver injury caused by Escherichia coli infection in mice

Takashi Hiromatsu, Tetsuya Matsuguchi, Hideyuki Shimizu, Toshiki Yaijima, Hitoshi Nishimura, Toshiyuki Arai, Yuji Nimura, Yasunobu Yoshika

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    Fas ligand (Fas L) expression was induced on intrahepatic NK1.1+ T cells in vivo after an intraperitoneal inoculation of Escherichia coli. Liver injury after E. coli infection, as assessed by serum GPT level and histological examination, was significantly reduced in Jα281-/- mice lacking NK1.1+ T cells or in gld/gld mice bearing mutated Fas L, indicating that NK T cells at least partly contribute to E. coli-induced liver injury in a Fas/Fas L-dependent manner. Bacterial numbers in organs and cytokine levels in serum of Jα281-/- mice did not differ from those of Jα281+/+ mice following E. coli infection. Intrahepatic NK1.1+ T cells, which preferentially expressed Toll-like receptor 2 (TLR2) mRNA, responded in vitro to synthetic lipoprotein, a ligand for TLR2, by inducing Fas L expression on their surface. In a manner analogous to E. coli infection, lipoprotein and LPS could additively induce Fas L expression on NK1.1+ T cells, leading to liver injury in vivo in normal mice but not in gld/gld mice. In conclusion, it is suggested that induction of Fas L on NK T cells in response to bacterial components such as lipoproteins plays an important role in pathogenesis of E. coli-induced liver injury in mice.

    Original languageEnglish
    Pages (from-to)2511-2519
    Number of pages9
    JournalEuropean Journal of Immunology
    Issue number9
    Publication statusPublished - Sep 1 2003


    All Science Journal Classification (ASJC) codes

    • Immunology and Allergy
    • Immunology

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