Journal
NATURE REVIEWS IMMUNOLOGY
Volume 17, Issue 7, Pages 421-436Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nri.2017.24
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Funding
- National Heart, Lung, and Blood Institute
- National Institute of Diabetes and Digestive and Kidney Diseases
- National Institute of Allergy and Infectious Diseases of the US National Institutes of Health (NIH) [R01HL075453, R01A1084457, R01A1071163, DP3DK097672, DP3DK111802, DP3DK097672-01S1, T32AI106677, K08AI112993]
- Benaroya Family Gift Fund
- Howard Hughes Medical Institute-NIH Molecular Medicine Training Grant
- American College of Rheumatology Research and Education Foundation Rheumatology Scientist Development Award
- Arthritis National Research Foundation
- Novel Research Grant from Lupus Research Alliance
- Arnold Lee Smith Endowed Professorship for Research Faculty Development
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Recent work has provided new insights into how altered B cell-intrinsic signals through the B cell receptor (BCR) and key co-receptors - function together to promote the pathogenesis of autoimmunity. These combined signals affect B cells at two distinct stages: first, in the selection of the naive repertoire; and second, during extrafollicular or germinal centre activation responses. Thus, dysregulated signalling can lead to both an altered naive BCR repertoire and the generation of autoantibody-producing B cells. Strikingly, high-affinity autoantibodies predate and predict disease in several autoimmune disorders, including type 1 diabetes and systemic lupus erythematosus. This Review summarizes how, rather than being a downstream consequence of autoreactive T cell activation, dysregulated B cell signalling can function as a primary driver of many human autoimmune diseases.
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