LFA-1/ICAM-1 interaction lowers the threshold of B cell activation by facilitating B cell adhesion and synapse formation
LFA-1/ICAM-1 interaction lowers the threshold of B cell activation by facilitating B cell adhesion and synapse formation
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DOI：
10.1016/s1074-7613(04)00105-0
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发表时间：
2004-05-01
期刊：
影响因子：
32.4
通讯作者：
Batista, FD
中科院分区：
文献类型：
--
作者：
Carrasco, YR;Fleire, SJ;Batista, FD
整合素LFA-1及其配体ICAM-1介导B细胞黏附，但其在膜结合抗原识别中的作用尚不清楚。在这里，利用平面脂质双层和表达ICAM-1的细胞融合绿色荧光蛋白，我们发现B细胞受体(BCR)的结合通过LFA-1介导的机制促进B细胞的黏附。LFA-1被招募来形成一个成熟的B细胞突触，分离成一个围绕BCR的环。这种分布在BCR/抗原亲和力的大范围内(10(6)M-1到10(11)M-1)保持不变。此外，LFA-1与ICAM-1的结合降低了形成突触和触发B细胞所需的抗原水平。因此，LFA-1/ICAM-1相互作用通过促进B细胞黏附和突触形成来降低B细胞激活的阈值。
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.