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suck abstract from ncbi


10.1016/j.cca.2008.05.012

http://scihub22266oqcxt.onion/10.1016/j.cca.2008.05.012
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18538665!ä!18538665

suck abstract from ncbi


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pmid18538665      Clin+Chim+Acta 2008 ; 395 (1-2): 77-83
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  • Up-regulation of adhesion molecule expression and induction of TNF-alpha on vascular endothelial cells by antibody against human parvovirus B19 VP1 unique region protein #MMPMID18538665
  • Tzang BS; Tsai CC; Chiu CC; Shi JY; Hsu TC
  • Clin Chim Acta 2008[Sep]; 395 (1-2): 77-83 PMID18538665show ga
  • BACKGROUND: Human parvovirus B19 infection has been frequently described as a cause or trigger of various autoimmune diseases. In previous studies, we have postulated the association among human parvovirus B19 (B19)-VP1 unique region (VP1u), production of anti-beta2-glycoprotein I (anti-beta2GPI) antibody and anti-phospholipid syndrome (APS)-like autoimmunity. However, the precise role of B19-VP1u in induction of APS is still obscure. METHODS: To further elucidate the pathogenic roles of VP1u in B19 infection and autoimmunity, we examined the effect of anti-B19-VP1u IgG antibodies on endothelial cells that is recognized to play crucial roles in APS. Human vascular endothelial cells, ECV-304, were incubated with various preparations of purified human or rabbit IgG. The activation of endothelial cells and production of cytokines were assessed by flow cytometry and ELISA, respectively. RESULTS: Purified IgG from rabbits immunized with recombinant B19-VP1u proteins can up-regulate ICAM-1 (CD54), VCAM-1 (CD106), E-selectin (CD62E), MHC class II (HLA-DR, DP, DQ) molecule expression, and TNF-alpha production in endothelial cells as compared to those endothelial cells cultured with control IgG. Additionally, significantly increased phosphorylated-P38 mitogen-activated protein kinase (P38 MAPK) and iNOS were observed in both human anti-beta2GPI IgG and rabbit anti-B19-VP1u IgG treated-ECV-304 cells, respectively. CONCLUSIONS: These experimental results imply that antibodies against B19-VP1u play important roles in the immunopathological processes as well as human anti-beta2GPI IgG that leads to development of APS by involving p38 phosphorylation and iNOS activation. It could provide a clue in understanding the role of anti-B19-VP1u antibodies in APS manifestations.
  • |Animals[MESH]
  • |Capsid Proteins/*immunology[MESH]
  • |Cell Adhesion Molecules/*biosynthesis[MESH]
  • |Cells, Cultured[MESH]
  • |Endothelium, Vascular/cytology/*immunology/virology[MESH]
  • |Humans[MESH]
  • |Immunoglobulin G/*blood[MESH]
  • |Nitric Oxide Synthase Type II/metabolism[MESH]
  • |Parvoviridae Infections/immunology[MESH]
  • |Parvovirus B19, Human/*immunology[MESH]
  • |Phosphorylation[MESH]
  • |Rabbits[MESH]
  • |Tumor Necrosis Factor-alpha/*biosynthesis[MESH]
  • |Up-Regulation[MESH]


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