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PILRα negatively regulates mouse inflammatory arthritis.
Sun, Yonglian; Caplazi, Patrick; Zhang, Juan; Mazloom, Anita; Kummerfeld, Sarah; Quinones, Gabriel; Senger, Kate; Lesch, Justin; Peng, Ivan; Sebrell, Andrew; Luk, Wilman; Lu, Yanmei; Lin, Zhonghua; Barck, Kai; Young, Judy; Del Rio, Mariela; Lehar, Sophie; Asghari, Vida; Lin, WeiYu; Mariathasan, Sanjeev; DeVoss, Jason; Misaghi, Shahram; Balazs, Mercedesz; Sai, Tao; Haley, Benjamin; Hass, Philip E; Xu, Min; Ouyang, Wenjun; Martin, Flavius; Lee, Wyne P; Zarrin, Ali A.
Afiliación
  • Sun Y; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Caplazi P; Department of Pathology, Genentech, South San Francisco, CA 94080;
  • Zhang J; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Mazloom A; Department of Protein Chemistry, Genentech, South San Francisco, CA 94080;
  • Kummerfeld S; Department of Bioinformatics and Computational Biology, Genentech, South San Francisco, CA 94080;
  • Quinones G; Department of Protein Chemistry, Genentech, South San Francisco, CA 94080;
  • Senger K; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Lesch J; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Peng I; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Sebrell A; Department of Antibody Engineering, Genentech, South San Francisco, CA 94080;
  • Luk W; Department of Biochemical and Cellular Pharmacology, Genentech, South San Francisco, CA 94080;
  • Lu Y; Department of Biochemical and Cellular Pharmacology, Genentech, South San Francisco, CA 94080;
  • Lin Z; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Barck K; Department of Biomedical Imaging, Genentech, South San Francisco, CA 94080;
  • Young J; Department of Biochemical and Cellular Pharmacology, Genentech, South San Francisco, CA 94080;
  • Del Rio M; Department of Transgenic Technology, Genentech, South San Francisco, CA 94080;
  • Lehar S; Department of Microbial Pathogenesis, Genentech, South San Francisco, CA 94080; and.
  • Asghari V; Department of Transgenic Technology, Genentech, South San Francisco, CA 94080;
  • Lin W; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Mariathasan S; Department of Microbial Pathogenesis, Genentech, South San Francisco, CA 94080; and.
  • DeVoss J; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Misaghi S; Department of Early Stage Cell Culture, Genentech, South San Francisco, CA 94080.
  • Balazs M; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Sai T; Department of Antibody Engineering, Genentech, South San Francisco, CA 94080;
  • Haley B; Department of Protein Chemistry, Genentech, South San Francisco, CA 94080;
  • Hass PE; Department of Protein Chemistry, Genentech, South San Francisco, CA 94080;
  • Xu M; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Ouyang W; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Martin F; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Lee WP; Department of Immunology, Genentech, South San Francisco, CA 94080;
  • Zarrin AA; Department of Immunology, Genentech, South San Francisco, CA 94080; zarrin.ali@gene.com.
J Immunol ; 193(2): 860-70, 2014 Jul 15.
Article en En | MEDLINE | ID: mdl-24935926
Paired Ig-like type 2 receptor (PILR)α inhibitory receptor and its counterpart PILRß activating receptor are coexpressed on myeloid cells. In this article, we report that PILRα, but not PILRß, 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.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Artritis Experimental / Receptores Inmunológicos / Citocinas / Inflamación Idioma: En Revista: J Immunol Año: 2014 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Artritis Experimental / Receptores Inmunológicos / Citocinas / Inflamación Idioma: En Revista: J Immunol Año: 2014 Tipo del documento: Article Pais de publicación: Estados Unidos