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IL-17 Signaling-Independent Central Nervous System Autoimmunity Is Negatively Regulated by TGF-β¹

Ines Gonzalez-García^2,*, Yani Zhao^2,*, Songguang Ju^*, Qin Gu^*, Lin Liu^*, Jay K. Kolls and Binfeng Lu^3,*,

^* Department of Immunology, University of Pittsburgh School of Medicine; University of Pittsburgh Cancer Institute; Department of Pediatrics, and Division of Pulmonary Medicine, Allergy, and Immunology, Children’s Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261

Recent studies have established an important role of Th17 in induction of autoimmune diseases. We have found that although IL-17 receptor A (IL-17RA)^–/– mice were resistant to experimental autoimmune encephalomyelitis, a small number of them developed milder clinical signs of this autoimmune disease. In addition, blockade of TGF-β in IL-17RA^–/– mice resulted in much more severe clinical signs of experimental autoimmune encephalomyelitis and significantly increased parenchymal lymphocyte infiltration in the CNS. Furthermore, the number of autoreactive Th1 cells was greatly increased in the inflamed spinal cord of IL-17RA^–/– mice. These data support a role of IL-17RA-independent mechanisms in causing autoimmunity and its regulation by TGF-β.

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 is partly supported by National Institutes of Health (NIH) Grant No. AI063496 (to B.L.). B.L. is supported by National Institutes of Health Grant No.1 K01 AR048854. Y.Z. was partly supported by National Institutes of Health Grant No. P30-AR47372.

² I.G.-G. and Y.Z. contributed equally to this article.

³ Address correspondence and reprint requests to Dr. Binfeng Lu, University of Pittsburgh, 200 Iothrop Street, Pittsburgh, PA 15261. E-mail address: Binfeng{at}pitt.edu

⁴ Abbreviations used in this paper: EAE, experimental autoimmune encephalomyelitis; IL-17RA, IL-17 receptor A; WT, wild type.

⁵ The online version of this article contains supplementary material.