The Journal of Experimental Medicine
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Published online 11 September 2006 doi:10.1084/jem.20061446
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 10, 2255-2261
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BRIEF DEFINITIVE REPORT

Persistent expression of autoantibodies in SLE patients in remission

Sergey Yurasov1,2, Thomas Tiller3, Makoto Tsuiji1, Klara Velinzon1, Virginia Pascual4, Hedda Wardemann3, and Michel C. Nussenzweig5

1 Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10021
2 Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New York, NY 10021
3 Max-Planck Institute for Infection Biology, D-10117 Berlin, Germany
4 Baylor Institute for Immunology Research, Dallas, TX 75204
5 Howard Hughes Medical Institute New York, NY 10021

CORRESPONDENCE Hedda Wardemann: wardemann{at}mpiib-berlin.mpg.de OR Michel C. Nussenzweig: nussen{at}mail.rockefeller.edu

A majority of the antibodies expressed by nascent B cells in healthy humans are self-reactive, but most of these antibodies are removed from the repertoire during B cell development. In contrast, untreated systemic lupus erythematosus (SLE) patients fail to remove many of the self-reactive and polyreactive antibodies from the naive repertoire. Here, we report that SLE patients in clinical remission continue to produce elevated numbers of self-reactive and polyreactive antibodies in the mature naive B cell compartment, but the number of B cells expressing these antibodies is lower than in patients with active disease. Our finding that abnormal levels of self-reactive mature naive B cells persist in the majority of patients in clinical remission suggests that early checkpoint abnormalities are an integral feature of SLE.


H. Wardemann and M.C. Nussenzweig contributed equally to this work.


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