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T Cell Differentiation Leads to Default Production of IFN-: Failure to Down-Regulate IL-12 Receptor ß2-Chain Expression1
Sections of
*
Rheumatology and
Pulmonary and Critical Care Medicine, Department of Medicine,
Department of Pathology, and
§
Section of Immunobiology, Yale School of Medicine, New Haven, CT 06520
T cells secrete Th1- and Th2-like cytokines that help
mediate innate and acquired immunity. We have addressed the mechanism
whereby murine T cells acquire the capacity to differentially
produce such cytokines. Splenic T cells could be polarized into
IFN-- or IL-4-secreting cells in vitro; however, in contrast to
CD4+ 
ß T cells, T cells predominantly produced
IFN-, even in the presence of IL-4, a finding independent of genetic
background. Like CD4+ Th1 cells, IFN--producing cells
expressed the IL-12 receptor ß2-chain after activation in
the presence of IL-12; however, unlike Th2 cells, IL-4-primed T
cells also expressed this receptor, even in the absence of IFN- and
despite the presence of the transcription factor GATA-3. IL-12 also
induced IL-4-primed T cells to proliferate and to translocate
Stat3/Stat4, indicating signaling through the IL-12 receptor. These
molecular events can account for the predominant production of IFN-
by T cells in the presence of IL-12, despite the availability of
IL-4. Early and predominant production of IFN- by T cells
likely is critical for the roles that these cells play in protection
against intracellular pathogens and in tumor
immunity.
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