Activation of T cells recognizing an epitope of heat-shock protein 70 can protect against rat adjuvant arthritis

Shigehisa Tanaka, Yuki Kimura, Akio Mitani, Genta Yamamoto, Hitoshi Nishimura, Ralf Spallek, Mahavir Singh, Toshihide Noguchi, Yasunobu Yoshikai

    研究成果: Contribution to journalArticle査読

    71 被引用数 (Scopus)

    抄録

    We have previously reported that CD4+ T cells recognizing a peptide comprising residues 234-252 of the heat shock protein (HSP)70 of Mycobacterium tuberculosis (M.tb) in the context of RT1.B MHC class H molecule emerged in the peritoneal cavity during the course of Listeria monocytogenes infection in rats and suppressed the inflammatory responses against listerial infection via IL-10 production. We report in this work that pretreatment with peptide 234-252 of HSP70 derived from M.tb suppressed the development of adjuvant arthritis (AA) in Lewis rats induced using heat- killed M.tb. T cells from rats pretreated with peptide 234-252 produced a significant amount of IL-10 in response to the epitope. T cells from rats pretreated with the peptide and immunized with M.tb produced the larger amount of IL-10 in response to the peptide, but only a marginal level of IFN- γ in response to purified protein derivative of M.tb. Administration of anti-IL-10 Ab partly inhibited the suppressive effect of pretreatment with peptide 234-252 on the development of AA. Furthermore, transfer of a T cell line specific for the epitope at the time of AA induction markedly suppressed AA. These findings suggested that T cells recognizing peptide 234-252 may play a regulatory role in inflammation during AA via the production of suppressive cytokines including IL-10.

    本文言語英語
    ページ(範囲)5560-5565
    ページ数6
    ジャーナルJournal of Immunology
    163
    10
    出版ステータス出版済み - 11 15 1999

    All Science Journal Classification (ASJC) codes

    • 免疫アレルギー学
    • 免疫学

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