Mac-1 promotes FcgammaRIIA-dependent cell spreading and migration on immune complexes.
Mac-1 promotes FcgammaRIIA-dependent cell spreading and migration on immune complexes.
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Mac-1 促进 FcgammaRIIA 依赖性细胞在免疫复合物上的扩散和迁移。
DOI：
10.1021/bi060529u
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发表时间：
2006
期刊：
影响因子：
2.9
通讯作者：
Zhang,Li
中科院分区：
文献类型：
--
作者：
Xiong,Ying;Cao,Chunzhang;Makarova,Alexandra;Hyman,Brad;Zhang,Li
The integrin Mac-1 plays a critical role in Fc receptor (FcR)-mediated antibody-dependent cellular cytotoxicity (ADCC). However, the mechanism by which Mac-1 facilitates the functions of FcγRIIA, a major FcR expressed on human leukocytes, is not fully understood. We report here that Mac-1 sustains cell adhesion, enhances cell spreading, and accelerates cell migration on preformed immune complexes (ICs) by directly interacting with FcγRIIA but not with the IC substrate. Coupling Mac-1 to FcγRIIA allows FcγRIIA to reside in the leading front of actin polymerization at the filopodial extension and thus could potentially enhance FcγRIIA-mediated cell spreading and migration. The direct interaction between Mac-1 and FcγRIIA is demonstrated by co-immunoprecipitation, by cell surface co-localization, and by solid-phase binding assays using recombinant αMI-domain and soluble FcγRIIA. Further mutational analysis identifies the E253-R261sequence within the αMI-domain as part of the FcγRIIA binding interface within Mac-1. Altogether, these results demonstrate that FcγRIIA recognizes Mac-1 via the αMI-domain but not the lectin domain, a distinct feature from other FcRs, and that Mac-1 binding confers FcγRIIA with the ability to prolong cell adhesion as well as to spread and migrate on the ICs, leading to effective cell killing by ADCC.
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