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Identification of two major autoantigens negatively regulating endothelial activation in Takayasu arteritis.

Nature communications (2020-03-11)
Tomoyuki Mutoh, Tsuyoshi Shirai, Tomonori Ishii, Yuko Shirota, Fumiyoshi Fujishima, Fumiaki Takahashi, Yoichi Kakuta, Yoshitake Kanazawa, Atsushi Masamune, Yoshikatsu Saiki, Hideo Harigae, Hiroshi Fujii
ABSTRACT

The presence of antiendothelial cell antibodies (AECAs) has been documented in Takayasu arteritis (TAK), a chronic granulomatous vasculitis. Here, we identify cell-surface autoantigens using an expression cloning system. A cDNA library of endothelial cells is retrovirally transfected into a rat myeloma cell line from which AECA-positive clones are sorted with flow cytometry. Four distinct AECA-positive clones are isolated, and endothelial protein C receptor (EPCR) and scavenger receptor class B type 1 (SR-BI) are identified as endothelial autoantigens. Autoantibodies against EPCR and SR-BI are detected in 34.6% and 36.5% of cases, respectively, with minimal overlap (3.8%). Autoantibodies against EPCR are also detected in ulcerative colitis, the frequent comorbidity of TAK. In mechanistic studies, EPCR and SR-BI function as negative regulators of endothelial activation. EPCR has also an effect on human T cells and impair Th17 differentiation. Autoantibodies against EPCR and SR-BI block the functions of their targets, thereby promoting pro-inflammatory phenotype.

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Sigma-Aldrich
Anti-Human IgG (Fab specific)−FITC antibody produced in goat, affinity isolated antibody, buffered aqueous solution

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