Qian Kun, Xie Fenglong, Gibson Andrew W, Edberg Jeffrey C, Kimberly Robert P, Wu Jianming
Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, 202 Shelby Interdisciplinary Biomedical Science Building, 1825 University Boulevard, Birmingham, AL 35294-2182, USA.
J Leukoc Biol. 2008 Dec;84(6):1492-500. doi: 10.1189/jlb.0508327. Epub 2008 Sep 10.
FcalphaRI (CD89) is a human IgA FcR expressed on cells of myeloid lineage such as neutrophils, monocytes, tissue macrophages, eosinophils, and subpopulations of dendritic cells. FcalphaRI mediates cell activation through Src family kinases and downstream tyrosine-based phosphorylation pathways. However, the role of IgA and the expression and role of its cognate receptor FcalphaRI (CD89) in platelet activation are undefined. In the current study, we demonstrate that human platelets express FcalphaRI mRNAs and proteins. Furthermore, we show that the platelet FcalphaRI is associated with the FcR gamma-chain, and cross-linking of FcalphaRI leads to Syk phosphorylation. Clustering of FcalphaRI induces pre-mRNA splicing and protein production of tissue factor and IL-1beta, suggesting novel roles for human platelet FcalphaRI and serum IgA in thrombosis and inflammation.
FcalphaRI(CD89)是一种在髓系谱系细胞(如中性粒细胞、单核细胞、组织巨噬细胞、嗜酸性粒细胞和树突状细胞亚群)上表达的人IgA Fc受体。FcalphaRI通过Src家族激酶和下游基于酪氨酸的磷酸化途径介导细胞活化。然而,IgA及其同源受体FcalphaRI(CD89)在血小板活化中的作用尚不清楚。在本研究中,我们证明人血小板表达FcalphaRI mRNA和蛋白。此外,我们表明血小板FcalphaRI与FcRγ链相关,FcalphaRI的交联导致Syk磷酸化。FcalphaRI的聚集诱导组织因子和IL-1β的前体mRNA剪接和蛋白产生,提示人血小板FcalphaRI和血清IgA在血栓形成和炎症中具有新的作用。