PILRα Negatively Regulates Mouse Inflammatory Arthritis
Author(s) -
Yonglian Sun,
Patrick Caplazi,
Juan Zhang,
Anita Mazloom,
Sarah Kummerfeld,
Gabriel A. Quiñones,
Kate Senger,
Justin Lesch,
Ivan Peng,
Andrew Sebrell,
Wilman Luk,
Yanmei Lu,
Zhonghua Lin,
Kai Barck,
Judy Young,
Mariela Del Rio,
Sophie M. Lehar,
Vida Asghari,
WeiYu Lin,
Sanjeev Mariathasan,
Jason DeVoss,
Shahram Misaghi,
Mercedesz Balázs,
Tao Sai,
Benjamin Haley,
Philip E. Hass,
Min Xu,
Wenjun Ouyang,
Flavius Martin,
Wyne P. Lee,
Ali A. Zarrin
Publication year - 2014
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.1400045
Subject(s) - arthritis , inflammatory arthritis , immunology , microbiology and biotechnology , biology
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.
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