CD22: A Regulator of Innate and Adaptive B Cell Responses and Autoimmunity

被引：147

作者：

Clark, Edward A. ^{[1
,2
]}

Giltiay, Natalia V. ^{[2
]}

机构：

[1] Univ Washington, Dept Immunol, Seattle, WA 98195 USA

[2] Univ Washington, Dept Med, Div Rheumatol, Seattle, WA 98195 USA

来源：

FRONTIERS IN IMMUNOLOGY | 2018年 / 9卷

关键词：

CD22; B cells; autoimmunity; antigens; TLR7; T cell dependent; T cell independent; SYSTEMIC-LUPUS-ERYTHEMATOSUS; PROTEIN-TYROSINE-PHOSPHATASE; RECEPTOR SIGNAL-TRANSDUCTION; HIGH-AFFINITY AUTOANTIBODIES; IN-VIVO SUBSTRATE; ANTIGEN RECEPTOR; CD22-DEFICIENT MICE; MEDIATED REGULATION; DENDRITIC CELLS; CROSS-LINKING;

D O I：

10.3389/fimmu.2018.02235

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

CD22 (Siglec 2) is a receptor predominantly restricted to B cells. It was initially characterized over 30 years ago and named "CD22" in 1984 at the 2nd International workshop in Boston (1). Several excellent reviews have detailed CD22 functions, CD22-regulated signaling pathways and B cell subsets regulated by CD22 or Siglec G (2-4). This review is an attempt to highlight recent and possibly forgotten findings. We also describe the role of CD22 in autoimmunity and the great potential for CD22-based immunotherapeutics for the treatment of autoimmune diseases such as systemic lupus erythematosus (SLE).

引用

页数：13

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