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Prepublished online as a Blood First Edition Paper on April 17, 2002; DOI 10.1182/blood-2002-01-0027. This Article Full Text (PDF) All Versions of this Article: 2002-01-0027v1 100/1/184    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Jackson, D. E Articles by Bartley, P. A Search for Related Content PubMed PubMed Citation Articles by Jackson, D. E Articles by Bartley, P. A Social Bookmarking                   What's this? Submitted January 8, 2002 Accepted February 28, 2002 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 Denise E Jackson*, Ray Wilkinson, Bruce A Lyons, Mae-Xhum Wong, Donna Roberts, and Paul A Bartley * Corresponding author; email: denise.jackson{at}imvs.sa.gov.au. Platelet Endothelial Cell Adhesion Molecule-1 (PECAM-1/CD31) is an 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 hyper-responsive 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 hyper-proliferative responses to lipopolysaccharide and anti-IgM stimulation and showed enhanced kinetics in their intracellular Ca2+ response following IgM cross-linking. PECAM-1-/- mice showed increased serum levels of IgM with elevated IgG isotypes and IgA anti-DNP antibody in response to the T-independent antigen, DNP-Ficoll. Finally, PECAM-1-/- mice developed anti-nuclear antibodies and lupus-like autoimmune disease with age. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Wu, K. Tworkoski, M. Michaud, and J. A. Madri Bone Marrow Monocyte PECAM-1 Deficiency Elicits Increased Osteoclastogenesis Resulting in Trabecular Bone Loss J. Immunol., March 1, 2009; 182(5): 2672 - 2679. [Abstract] [Full Text] [PDF] N. Sugimoto, T. Rui, M. Yang, S. Bharwani, O. Handa, N. Yoshida, T. Yoshikawa, and P. R. Kvietys Points of Control Exerted along the Macrophage-Endothelial Cell-Polymorphonuclear Neutrophil Axis by PECAM-1 in the Innate Immune Response of Acute Colonic Inflammation J. Immunol., August 1, 2008; 181(3): 2145 - 2154. [Abstract] [Full Text] [PDF] C. Bergom, C. Paddock, C. Gao, T. Holyst, D. K. Newman, and P. J. Newman An alternatively spliced isoform of PECAM-1 is expressed at high levels in human and murine tissues, and suggests a novel role for the C-terminus of PECAM-1 in cytoprotective signaling J. Cell Sci., April 15, 2008; 121(8): 1235 - 1242. [Abstract] [Full Text] [PDF] Y. Rui, X. Liu, N. Li, Y. Jiang, G. Chen, X. Cao, and J. Wang PECAM-1 Ligation Negatively Regulates TLR4 Signaling in Macrophages J. Immunol., December 1, 2007; 179(11): 7344 - 7351. [Abstract] [Full Text] [PDF] R. Goel, B. Boylan, L. Gruman, P. J. Newman, P. E. North, and D. K. 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