炎症
脱颗粒
免疫学
补体系统
Arthus反应
免疫系统
趋化性
受体
抗体
免疫复合物
C5a受体
外渗
化学
医学
生物化学
作者
Rangaiah Shashidharamurthy,Randolph A. Hennigar,Sébastien Fuchs,Purani Palaniswami,Melanie A. Sherman,Periasamy Selvaraj
出处
期刊:Blood
[American Society of Hematology]
日期:2008-01-15
卷期号:111 (2): 894-904
被引量:38
标识
DOI:10.1182/blood-2007-04-085944
摘要
Extravasation and emigration of neutrophils to the site of inflammation are essential early steps in the initiation of many antibody-mediated autoimmune diseases. The Fc domains of cell bound autoantibodies or immune-complexes (IC) are capable of triggering the neutrophil emigration via complement and FcγRs-mediated mechanisms. To define the clinical relevance and the relative contribution of these 2 pathways in IC-mediated neutrophil emigration, we have neutralized the FcγR-binding activity of IC with a recombinant dimeric Fc receptor, CD16A-Ig, and investigated the early events of IC-induced inflammation in mice. Systemic administration of purified CD16A-Ig blocked IC-induced inflammation, mast- cell degranulation, and extravasation of neutrophils in a reversed Arthus reaction. Although the binding of CD16A-Ig to IC did not alter the complement-activating properties of IC, no evidence for complement-dependent neutrophil emigration was observed. These results suggest that interaction of IC with cells expressing FcγRs at the inflammatory site results in the secretion of chemoattractants, which mediate complement-independent emigration of neutrophils in this cutaneous acute inflammation model. Furthermore, blocking the interaction of IC to FcγRs expressed on inflammatory cells by administering high-avidity Fc fusion dimers of low-affinity FcγRs is an effective way of preventing IC-induced acute inflammation in autoimmune diseases.
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