
This study was undertaken to investigate the role of CD52 in monocyte adhesion and type I IFN signaling in patients with SSc. The impact of overexpression, knockdown, and antibody blocking of CD52 was analyzed by gene and protein expression assays and functional assays. Changes in CD52 expression were consistent with the SSc subtypes, as well as with immunosuppressive treatments, autoantibody profiles, and monocyte adhesion properties in patients with SSc. Experiments with the humanized anti CD52 monoclonal antibody alemtuzumab in blood samples from healthy controls increased monocyte adhesion and CD11b/CD18 expression, and enhanced type I IFN responses. Targeting of the IFN HDAC CD52 axis in monocytes might represent a new therapeutic option for patients with early SSc.
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