Cutting edge: IFN-γ enables APC to promote memory Th17 and Abate Th1 cell development

Ilona Kryczek, Shuang Wei, Wenrong Gong, Xiaogong Shu, Wojciech Szeliga, Linhua Vatan, Lieping Chen, Guobin Wang, Weiping Zou

Research output: Contribution to journalArticlepeer-review

Abstract

Th1-derived IFN-γ targets naive T cells and inhibits Th17 development. However, Th1, Th17, and memory but not naive T cells are colocalized in an inflammatory environment. To demonstrate the kinetic relationship between these T cell subsets, we investigated the role of IFN-γ in regulating the development and balance between Th17 and Th1 in humans. We show that IFN-γ stimulates B7-H1 expression on APC subsets and abates their Th1 polarization capacity in a B7-H1-dependent manner. Interestingly, IFN-γ triggers APCs to produce IL-1 and IL-23 and enables them to induce memory Th17 expansion via IL-1 and IL-23 in a B7-H1-independent manner. We propose a novel dynamic between Th1 and Th17 in the course of inflammation as follows: Th1-mediated inflammation is attenuated by IFN-γ-induced B7-H1 on APCs and is evolved toward Th17-mediated chronic inflammation by IFN-γ-induced, APC-derived IL-1 and IL-23. Our study challenges the dogma that IFN-γ suppresses Th17 and enhances Th1 development.

Original languageEnglish (US)
Pages (from-to)5842-5846
Number of pages5
JournalJournal of Immunology
Volume181
Issue number9
StatePublished - Nov 1 2008

ASJC Scopus subject areas

  • Immunology
  • Medicine(all)

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