Resident Vδ1+ γδ T cells control early infiltration of neutrophils after Escherichia coli infection via IL-17 production

Kensuke Shibata, Hisakata Yamada, Hiromitsu Hara, Kenji Kishihara, Yasunobu Yoshikai

研究成果: ジャーナルへの寄稿記事

373 引用 (Scopus)

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Neutrophils infiltrate the site of infection and play critical roles in host defense, especially against extracellular bacteria. In the present study, we found a rapid and transient production of EL-17 after i.p. infection with Escherichia coli, preceding the influx of neutrophils. Neutralization of EL-17 resulted in a reduced infiltration of neutrophils and an impaired bacterial clearance. Ex vivo intracellular cytokine flow cytometric analysis revealed that γδ T cell population was the major source of EL-17. Mice depleted of γδ T cells by mAb treatment or mice genetically lacking Vδ1 showed diminished EL-17 production and reduced neutrophil infiltration after E. coli infection, indicating an importance of Vδ1+ γδ T cells as the source of IL-17. It was further revealed that γδ T cells in the peritoneal cavity of naive mice produced IL-17 in response to IL-23, which was induced rapidly after E. coli infection in a TLR4 signaling-dependent manner. Thus, although γδ T cells are generally regarded as a part of early induced immune responses, which bridge innate and adaptive immune responses, our study demonstrated a novel role of γδ T cells as a first line of host defense controlling neutrophil-mediated innate immune responses.

元の言語英語
ページ(範囲)4466-4472
ページ数7
ジャーナルJournal of Immunology
178
発行部数7
出版物ステータス出版済み - 4 1 2007

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All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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