BOR-SHOW TZANGTSAI-CHING HSU2026-10-162026-10-162008-09-01Pure ID: 14990646Pure UUID: 725a513b-6a97-4489-b3a5-5dfca89b2ba110.1016/j.cca.2008.05.012https://www.scopus.com/pages/publications/47749095519https://scholars.csmu.edu.tw/handle/123456789/23381Background: 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-β2GPI) 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-α 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-β2GPI 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-β2GPI 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.7enjournal article