| Literature DB >> 24935926 |
Yonglian Sun1, Patrick Caplazi2, Juan Zhang1, Anita Mazloom3, Sarah Kummerfeld4, Gabriel Quinones3, Kate Senger1, Justin Lesch1, Ivan Peng1, Andrew Sebrell5, Wilman Luk6, Yanmei Lu6, Zhonghua Lin1, Kai Barck7, Judy Young6, Mariela Del Rio8, Sophie Lehar9, Vida Asghari8, WeiYu Lin1, Sanjeev Mariathasan9, Jason DeVoss1, Shahram Misaghi10, Mercedesz Balazs1, Tao Sai5, Benjamin Haley3, Philip E Hass3, Min Xu1, Wenjun Ouyang1, Flavius Martin1, Wyne P Lee1, Ali A Zarrin11.
Abstract
Paired Ig-like type 2 receptor (PILR)α inhibitory receptor and its counterpart PILRβ activating receptor are coexpressed on myeloid cells. In this article, we report that PILRα, but not PILRβ, is elevated in human rheumatoid arthritis synovial tissue and correlates with inflammatory cell infiltration. Pilrα(-/-) mice produce more pathogenic cytokines during inflammation and are prone to enhanced autoimmune arthritis. Correspondingly, engaging PILRα with anti-PILRα mAb ameliorates inflammation in mouse arthritis models and suppresses the production of proinflammatory cytokines. Our studies suggest that PILRα mediates an important inhibitory pathway that can dampen inflammatory responses.Entities:
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Year: 2014 PMID： 24935926 DOI： 10.4049/jimmunol.1400045
Source DB: PubMed Journal: J Immunol ISSN： 0022-1767 Impact factor: 5.422