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Department of Molecular and Medical Pharmacology, University of California, Los Angeles, CA 90095
B cells can serve dual roles in modulating T cell immunity
through their potent capacity to present Ag and induce regulatory
tolerance. Although B cells are necessary components for the initiation
of spontaneous T cell autoimmunity to 
cell Ags in nonobese diabetic
(NOD) mice, the role of activated B cells in the autoimmune process is
poorly understood. In this study, we show that LPS-activated B cells,
but not control B cells, express Fas ligand and secrete TGF-.
Coincubation of diabetogenic T cells with activated B cells in vitro
leads to the apoptosis of both T and B lymphocytes. Transfusion of
activated B cells, but not control B cells, into prediabetic NOD mice
inhibited spontaneous Th1 autoimmunity, but did not promote Th2
responses to cell autoantigens. Furthermore, this treatment induced
mononuclear cell apoptosis predominantly in the spleen and temporarily
impaired the activity of APCs. Cotransfer of activated B cells with
diabetogenic splenic T cells prevented the adoptive transfer of type I
diabetes mellitus (T1DM) to NOD/scid mice. Importantly, whereas 90% of
NOD mice treated with control B cells developed T1DM within 27 wk,
<20% of the NOD mice treated with activated B cells became
hyperglycemic up to 1 year of age. Our data suggest that activated B
cells can down-regulate pathogenic Th1 immunity through triggering the
apoptosis of Th1 cells and/or inhibition of APC activity by the
secretion of TGF-. These findings provide new insights into T-B cell
interactions and may aid in the design of new therapies for human
T1DM.
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