第31回免疫学セミナーのお知らせ

演者：中江　進　先生

 Department of Pathology, Stanford University School of Medicine
理化学研究所　横浜研究所　免疫アレルギー科学総合研究センター
アレルギー遺伝子研究ユニット・研究員



平成19年 3月16日（金）
午後17：00-18：00

医学系学群棟　4A411

演題：「Mast cell-derived TNF promotes Th17 cell-dependent neutrophil-dominant airway inflammation」

要旨：IL-17 can contribute to host defense and autoimmunity, in part by orchestrating neutrophil recruitment. IL-17 also has been implicated in non-atopic asthma, in which the airway inflammation can include many neutrophils. We used ovalbumin-specific TCR-expressing C57BL/6-OTII mice to characterize the roles of mast cells and T cells in a new model of antigen (Ag)- and T cell-dependent airway neutrophilia. We found that Th17 cells and mast cells, but neither Th1 cells, Th2 cells nor antibody/Ag/FcRγ-signaling, contributed significantly to the Ag-dependent airway neutrophilia elicited in this model. Indeed, IFN-γ significantly suppressed IL-17-dependent airway neutrophilia in this setting. We detected no significant role for the candidate mast cell products histamine, PGD2, LTB4, CXCL10 or IL-16 in the neutrophil infiltration elicited in this model. By contrast, IL-18, IL-1βand TNF each contributed significantly to Th17 differentiation and the development of Ag- and Th17 cell-mediated airway neutrophilia. Moreover, we found that IL-17 enhanced mast cell-TNF production in vitro and that mast cell-associated TNF contributed significantly to Ag- and Th17 cell-mediated airway neutrophilia in vivo. These findings establish that mast cells can significantly enhance, by antibody- and FcRγg−independent mechanisms, an Ag- and Th17 cell-dependent inflammatory response that is characterized by neutrophil recruitment to the affected site.

問い合わせ先　：  人間総合科学研究科基礎医学系・
                          免疫学免疫学・渋谷　彰　 （ashibuya@md.tsukuba.ac.jp）
029-853-3281


たくさんのご来場お待ちしております。