期刊
EXPERT REVIEW OF CLINICAL IMMUNOLOGY
卷 12, 期 7, 页码 763-773出版社
TAYLOR & FRANCIS LTD
DOI: 10.1586/1744666X.2016.1152888
关键词
Bruton's tyrosine kinase; autoimmunity; B lymphocyte signaling; autoimmune inflammatory arthritis; type 1 diabetes; systemic lupus erythematosus; BTK inhibitors
类别
资金
- National Institutes of Health Grant: National Institute of Arthritis and Musculoskeletal and Skin Diseases [R01 AR049010]
- National Institutes of Health Grant: National Institute of Diabetes and Digestive and Kidney Diseases [R01 DK084246]
- National Institutes of Health Grant: National Institute of Heart, Lung and Blood [T32 HL069765]
Bruton's tyrosine kinase (BTK) mediates B cell signaling and is also present in innate immune cells but not T cells. BTK propagates B cell receptor (BCR) responses to antigen-engagement as well as to stimulation via CD40, toll-like receptors (TLRs), Fc receptors (FCRs) and chemokine receptors. Importantly, BTK can modulate signaling, acting as a rheostat rather than an on-off switch; thus, overexpression leads to autoimmunity while decreased levels improve autoimmune disease outcomes. Autoreactive B cells depend upon BTK for survival to a greater degree than normal B cells, reflected as loss of autoantibodies with maintenance of total antibody levels when BTK is absent. This review describes contributions of BTK to immune tolerance, including studies testing BTK-inhibitors for treatment of autoimmune diseases.
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