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Requirement of IL-17RA in Con A Induced Hepatitis and Negative Regulation of IL-17 Production in Mouse T Cells

Takako Nagata^*, Laura Mckinley^*, Jacques J. Peschon, John F. Alcorn^*, Shean J. Aujla^* and Jay K. Kolls^1,*

^* Children’s Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA 15213; and Institute for Systems Biology, Seattle, WA 98103

Th17 cells, a subset of T cells involved in autoimmunity and host defense against extracellular Gram-negative infection, express both IL-17A and IL-17F. Both IL-17A and IL-17F can signal via the IL-17RA; however, IL-17F does so at a 1- to 2-log higher concentration than IL-17A. In this study, we show that the IL-17F homodimer via IL-17RA is a negative regulator of IL-17 production in T cells and suggest a mechanism whereby IL-17RA on T cells serves as an autocrine/paracrine regulator of IL-17 synthesis in T cells.

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 Address correspondence and reprint requests to Dr. Jay K. Kolls, Children’s Hospital of Pittsburgh, Suite 3765, 3705 Fifth Avenue, Pittsburgh, PA 15213. E-mail address: jay.kolls{at}chp.edu

² Abbreviations used in this paper: KO, knockout; ALT, alanine aminotransferase; Ct, cycle threshold; WT, wild type.

³ The online version of this article contains supplemental material.

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