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Diabetes 54:2019-2025, 2005
© 2005 by the American Diabetes Association, Inc.

NOD B-cells Are Insufficient to Incite T-Cell-Mediated Anti-islet Autoimmunity

Daniel J. Moore1, Hooman Noorchashm2, Tina H. Lin2, Siri A. Greeley2, and Ali Naji2

1 Department of Pediatrics, Vanderbilt Children’s Hospital, Vanderbilt University, Nashville, Tennessee
2 Harrison Department of Surgical Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Although it is well established that B-cells are required for the development of diabetes in the nonobese diabetic (NOD) mouse, the nature of their role remains unknown. Herein, we investigate the hypothesis that B-cells in this autoimmune background actively disrupt the tolerant state of those T-cells with which they interact. We demonstrate that NOD B-cells express elevated levels of crucial molecules involved in antigen presentation (including CD21/35, major histocompatibility complex class II, and CD40), alterations that invite the possibility of inappropriate T-cell activation. However, when chimeric animals are generated in which all B-cells are NOD-derived, a tolerant state is maintained. These data demonstrate that although B-cells are required for the development of autoimmunity, they are not sufficient to disrupt established tolerance. Moreover, non-B-cell antigen-presenting cells may be the critical actors in the establishment of the tolerant state; this function may be absent in NOD mice as they are characterized by deficient professional antigen-presenting cell function.

Address correspondence and reprint requests to Ali Naji, 4 Silverstein Pavilion, Hospital of the University of Pennsylvania, Philadelphia, PA 19104. E-mail: alinaji{at}uphs.upenn.edu

Abbreviations: APC, antigen-presenting cell; CFSE, carboxyfluorescein diacetate succinimidyl ester; IMDM, Iscove’s modification of Dulbecco’s medium; MHC, major histocompatibility complex


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Copyright © 2005 by the American Diabetes Association.