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Annett M. Jacobi^a,b and Betty Diamond^a,b

^a A.M.J. is at Department of Rheumatology and Clinical Immunology, Charite University Hospital, 10117 Berlin, Germany.
^b B.D. is at Departments of Medicine and Microbiology, Columbia University Medical Center New York, NY 10032.

CORRESPONDENCE B.D.: bd2137{at}columbia.edu

Abstract
The autoimmune disease systemic lupus erythematosus (SLE) is caused by a failure of B cell tolerance. Recent studies in mouse models of SLE have identified several distinct tolerance checkpoints that must each function appropriately to protect against disease. However, studies of B cell repertoire selection in humans are essential to understand which checkpoints are defective in human autoimmune diseases.

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