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*
Department of Pathology and Center for Immunology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110; and
Department of Inflammation/Autoimmune Diseases, Hoffmann-La Roche, Inc., Nutley, NJ 07110; and
Dartmouth Medical School-DHMC, Department of Pathology, Lebanon, NH 03756
Expression of IL-12Rs is one important checkpoint for Th1
development. BALB/c DO11.10 CD4+ T cells stimulated by Ag
in neutral conditions lose expression of the IL-12R ß2 subunit and
become unresponsive to IL-12. In contrast, B10.D2 or F1
(BALB/c x B10.D2) DO11.10 CD4+ T cells maintain
IL-12Rß2 expression when stimulated similarly. Here we show that the
loss of IL-12 responsiveness by BALB/c T cells involves the action of
endogenous TGF-ß. BALB/c T cells stimulated in the presence of
anti-TGF-ß specifically maintain IL-12 responsiveness, express
IL-12Rß2 mRNA, and can stimulate nitric oxide production in
peritoneal exudate cells. Low concentrations of TGF-ß added
exogenously during primary activation of B10.D2 or F1 T
cells significantly inhibit their development of IL-12 responsiveness.
These effects of anti-TGF-ß are dependent on endogenous IFN-
and are inhibited by exogenously added IL-4. Thus, at least one effect
of TGF-ß on Th1/Th2 development may be the attenuation of IL-12Rß2
expression.
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