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Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84132. E-mail address: xinjian.chen@path.utah.edu
Despite the unequivocal role of B lymphocytes as effecter cells in humoral immunity, studies have reported that B cells are tolerogenic. The impact of B cell-mediated tolerance and its underlying mechanisms are incompletely understood. Using primary B cells as APCs and allogeneic CD4 T cells as responder cells in mixed leukocyte reactions, we find that B cells preferentially expand FoxP3+ over FoxP3– CD4 T cells in the absence of exogenous cytokines. The preferential expansion of Foxp3+ T cells is further enhanced by a partial blockade of class II MHC-TCR interaction but diminished by stimulatory anti-CD28 Ab or at high B to T cell ratios. Gamma irradiation of B cells selectively abrogates their ability to expand isolated CD25+ but not CD25– CD4 T cells; exogenous IL-2 supplement can partially restore this function. B cell-expanded CD25+ T cells express high levels of FoxP3 and are highly inhibitory in an Ag-specific manner.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 Address correspondence and reprint requests to Dr. Xinjian Chen, Department of Pathology, University of Utah School of Medicine, 1520 Emma Eccles Jones Building, 30 North 1900 East, Salt Lake City, UT 84132
2 Abbreviations used in this paper: MHC-II, MHC class II; B6, C57BL/6J; DC, dendritic cell; nTr, naturally occurring regulatory T (cell); Treg, regulatory T cell.
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