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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
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Zeitschriftentitel: | Blood |
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Personen und Körperschaften: | , , , , , |
In: | Blood, 100, 2002, 1, S. 184-193 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
American Society of Hematology
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Schlagwörter: |
author_facet |
Wilkinson, Ray Lyons, A. Bruce Roberts, Donna Wong, Mae-Xhum Bartley, Paul A. Jackson, Denise E. Wilkinson, Ray Lyons, A. Bruce Roberts, Donna Wong, Mae-Xhum Bartley, Paul A. Jackson, Denise E. |
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author |
Wilkinson, Ray Lyons, A. Bruce Roberts, Donna Wong, Mae-Xhum Bartley, Paul A. Jackson, Denise E. |
spellingShingle |
Wilkinson, Ray Lyons, A. Bruce Roberts, Donna Wong, Mae-Xhum Bartley, Paul A. Jackson, Denise E. Blood 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 Cell Biology Hematology Immunology Biochemistry |
author_sort |
wilkinson, ray |
spelling |
Wilkinson, Ray Lyons, A. Bruce Roberts, Donna Wong, Mae-Xhum Bartley, Paul A. Jackson, Denise E. 1528-0020 0006-4971 American Society of Hematology Cell Biology Hematology Immunology Biochemistry http://dx.doi.org/10.1182/blood-2002-01-0027 <jats:title>Abstract</jats:title><jats:p>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.</jats:p> 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 Blood |
doi_str_mv |
10.1182/blood-2002-01-0027 |
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Online Free |
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Biologie Medizin Chemie und Pharmazie |
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American Society of Hematology, 2002 |
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American Society of Hematology, 2002 |
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American Society of Hematology |
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49 |
title |
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 |
title_unstemmed |
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 |
title_full |
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 |
title_fullStr |
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 |
title_full_unstemmed |
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 |
title_short |
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 |
title_sort |
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 |
topic |
Cell Biology Hematology Immunology Biochemistry |
url |
http://dx.doi.org/10.1182/blood-2002-01-0027 |
publishDate |
2002 |
physical |
184-193 |
description |
<jats:title>Abstract</jats:title><jats:p>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.</jats:p> |
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author | Wilkinson, Ray, Lyons, A. Bruce, Roberts, Donna, Wong, Mae-Xhum, Bartley, Paul A., Jackson, Denise E. |
author_facet | Wilkinson, Ray, Lyons, A. Bruce, Roberts, Donna, Wong, Mae-Xhum, Bartley, Paul A., Jackson, Denise E., Wilkinson, Ray, Lyons, A. Bruce, Roberts, Donna, Wong, Mae-Xhum, Bartley, Paul A., Jackson, Denise E. |
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container_start_page | 184 |
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description | <jats:title>Abstract</jats:title><jats:p>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.</jats:p> |
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spelling | Wilkinson, Ray Lyons, A. Bruce Roberts, Donna Wong, Mae-Xhum Bartley, Paul A. Jackson, Denise E. 1528-0020 0006-4971 American Society of Hematology Cell Biology Hematology Immunology Biochemistry http://dx.doi.org/10.1182/blood-2002-01-0027 <jats:title>Abstract</jats:title><jats:p>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.</jats:p> 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 Blood |
spellingShingle | Wilkinson, Ray, Lyons, A. Bruce, Roberts, Donna, Wong, Mae-Xhum, Bartley, Paul A., Jackson, Denise E., Blood, 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, Cell Biology, Hematology, Immunology, Biochemistry |
title | 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 |
title_full | 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 |
title_fullStr | 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 |
title_full_unstemmed | 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 |
title_short | 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 |
title_sort | 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 |
title_unstemmed | 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 |
topic | Cell Biology, Hematology, Immunology, Biochemistry |
url | http://dx.doi.org/10.1182/blood-2002-01-0027 |