Platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) acts as a regulator of B-cell development, B-cell antigen receptor (BCR)-mediated activation, and autoimmune disease

被引：85

作者：

Wilkinson, R ^{[1
]}

Lyons, AB ^{[1
]}

Roberts, D ^{[1
]}

Wong, MX ^{[1
]}

Bartley, PA ^{[1
]}

Jackson, DE ^{[1
]}

机构：

[1] Inst Med & Vet Sci, Hanson Inst, Div Haematol, Adelaide, SA 5000, Australia

来源：

BLOOD | 2002年 / 100卷 / 01期

关键词：

D O I：

10.1182/blood-2002-01-0027

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) is an immunoglobulin-immunoreceptor tyrosine-based inhibitory motif (Ig-ITIM) superfamily member that recruits and activates protein-tyrosine phosphatases, SHP-1 and SHP-2, through its intrinsic ITIMs. PECAM-1-deficient (PECAM-1(-/-)) mice exhibit a hyperresponsive B-cell phenotype, increased numbers of B-1 cells, reduced B-2 cells, and develop autoantibodies. In the periphery, there are reduced mature recirculating B-2 cells and increased B-1a cells within the peritoneal cavity. In addition, PECAM-1(-/-) B cells display hyperproliferative responses to lipopolysaccharide and anti-IgM stimulation and showed enhanced kinetics in their intracellular Ca++ response following IgM cross-linking. PECAM-1(-/-) mice showed increased serum levels of IgM with elevated IgG isotypes and IgA antidinitrophenol antibody in response to the T-independent antigen, dinitrophenol-Ficoll. Finally, PECAM-1(-/-) mice developed antinuclear antibodies and lupuslike autoimmune disease with age.

引用

页码：184 / 193

页数：10

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