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Enables APC to Promote Memory Th17 and Abate Th1 Cell Development1
* Department of Surgery, University of Michigan, Ann Arbor, MI 48109;
Department of Surgery, Union Hospital, Wuhan, China; and
Department of Dermatology and Department of Oncology, Johns Hopkins University, Baltimore, MD 21231
Th1-derived IFN-
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- in regulating the development and balance between Th17 and Th1 in humans. We show that IFN- stimulates B7-H1 expression on APC subsets and abates their Th1 polarization capacity in a B7-H1-dependent manner. Interestingly, IFN- 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--induced B7-H1 on APCs and is evolved toward Th17-mediated chronic inflammation by IFN--induced, APC-derived IL-1 and IL-23. Our study challenges the dogma that IFN- suppresses Th17 and enhances Th1 development.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was partially supported by National Cancer Institute, National Institutes of Health Grants CA123088 and CA099985 (to W.Z.) and by the Marsha Rivkin Center for Ovarian Cancer Research (to I.K.).
2 Address correspondence and reprint requests to Dr. Weiping Zou, University of Michigan School of Medicine, 1150 West Medical Center Drive, Ann Arbor, MI 48109-0346. E-mail address: wzou{at}med.umich.edu
3 Abbreviations used in this paper: MDDC, monocyte-differentiated dendritic cell; siRNA, small interfering RNA.
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