期刊
IMMUNOLOGICAL REVIEWS
卷 307, 期 1, 页码 27-42出版社
WILEY
DOI: 10.1111/imr.13070
关键词
autoimmunity; B cells; protein kinases; phosphatases; signal transduction; tolerance; suppression; anergy
类别
资金
- National Institute of Health [AI149019]
This review article focuses on the B cell-intrinsic mechanisms that prevent the activation of autoreactive B cells in the periphery. It discusses the establishment of inhibitory signaling circuits, specifically the Lyn-SHIP-1-SHP-1 axis, and how disruptions of these circuits can contribute to the development of autoimmunity.
At least 20% of B cells in the periphery expresses an antigen receptor with a degree of self-reactivity. If activated, these autoreactive B cells pose a risk as they can contribute to the development of autoimmune diseases. To prevent their activation, both B cell-intrinsic and extrinsic tolerance mechanisms are in place in healthy individuals. In this review article, I will focus on B cell-intrinsic mechanisms that prevent the activation of autoreactive B cells in the periphery. I will discuss how inhibitory signaling circuits are established in autoreactive B cells, focusing on the Lyn-SHIP-1-SHP-1 axis, how they contribute to peripheral immune tolerance, and how disruptions of these circuits can contribute to the development of autoimmunity.
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