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CUTTING EDGE |
1
*
Department of Immunobiology, DNAX Research Institute, Palo Alto, CA 94304;
Wistar Institute, Philadelphia, PA 19104; and
Schering-Plough, Dardilly, France
The IL-12 receptor-ß2 (IL-12Rß2) chain is expressed on Th1
cells and lost upon differentiation to the Th2 phenotype. This has been
suggested as the basis for commitment of Th1 cells, because early
differentiated Th2 cells do not reverse their phenotype and do not
produce IFN-
on restimulation in the presence of IL-12. In this
study, we ectopically expressed the IL-12 receptor-ß2 (IL-12Rß2)
bicistronically with enhanced green fluorescent protein by retroviral
infection in developing and committed Th2 cells. Restimulation of Th2
cells expressing this ectopic IL-12Rß2 in the presence of IL-12 led
to levels of IL-4 production similar to those in control Th2 cells. The
expression of IL-12Rß2 in Th2 cells did not lead to significant
levels of IFN- production, although IL-12-mediated STAT signaling
and proliferation were restored. Thus, although the IL-12Rß2 and
IL-12-dependent STAT4 activation are required for Th1 responses,
activation of this pathway is not sufficient to restore a Th1 phenotype
in developing or committed Th2 cells.
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