CD22 and CD72 contribute to the development of scleroderma in a murine model

Systemic sclerosis (SSc) is characterized by vascular alterations and extensive fibrosis of the skin, lungs and other internal organs. Although the pathogenesis of SSc has not been elucidated, B cell abnormalities likely play an important role [1]. CD19, a B ‐cell‐specific cell surface molecule that defines signal thresholds critical for humoral immune responses and autoimmunity, is overexpressed on B cells from patients with SSc [2]. In the tight-skin (TSK/+) mouse, a genetic model for human SSc, TSK/+ mice deficient in CD19 expression demonstrated significantly decreased skin fibrosis [3].

Source: Journal of Dermatological Science - December 12, 2019 Category: Dermatology Authors: Chunyan Zhao, Takashi Matsushita, Vinh Thi Ha Nguyen, Momoko Tennichi, Manabu Fujimoto, Kazuhiko Takehara, Yasuhito Hamaguchi Source Type: research