LFA-1/ICAM-1 interaction lowers the threshold of B cell activation by facilitating B cell adhesion and synapse formation

被引:281
作者
Carrasco, YR
Fleire, SJ
Cameron, T
Dustin, ML
Batista, FD
机构
[1] Canc Res UK, London Res Inst, Lymphocyte Interact Lab, Lincolns Inn Fields Lab, London WC2A 3PX, England
[2] NYU, Sch Med, Dept Pathol, New York, NY 10016 USA
[3] Skirball Inst Biomol Med, Program Mol Pathogenesis, New York, NY 10016 USA
关键词
D O I
10.1016/S1074-7613(04)00105-0
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The integrin LFA-1 and its ligand ICAM-1 mediate B cell adhesion, but their role in membrane-bound antigen recognition is still unknown. Here, using planar lipid bilayers and cells expressing ICAM-1 fused to green fluorescence protein, we found that the engagement of B cell receptor (BCR) promotes B cell adhesion by an LFA-1-mediated mechanism. LFA-1 is recruited to form a mature B cell synapse segregating into a ring around the BCR. This distribution is maintained over a wide range of BCR/antigen affinities (10(6) M-1 to 10(11) M-1). Furthermore, the LFA-1 binding to ICAM-1 reduces the level of antigen required to form the synapse and trigger a B cell. Thus, LFA-1/ICAM-1 interaction lowers the threshold for B cell activation by promoting B cell adhesion and synapse formation.
引用
收藏
页码:589 / 599
页数:11
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