The IL-12 receptor-β2 (IL-12Rβ2) 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-γ on restimulation in the presence of IL-12. In this study, we ectopically expressed the IL-12 receptor-β2 (IL-12Rβ2) bicistronically with enhanced green fluorescent protein by retroviral infection in developing and committed Th2 cells. Restimulation of Th2 cells expressing this ectopic IL-12Rβ2 in the presence of IL-12 led to levels of IL-4 production similar to those in control Th2 cells. The expression of IL-12Rβ2 in Th2 cells did not lead to significant levels of IFN-γ production, although IL-12-mediated STAT signaling and proliferation were restored. Thus, although the IL-12Rβ2 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.
CITATION STYLE
Heath, V. L., Showe, L., Crain, C., Barrat, F. J., Trinchieri, G., & O’Garra, A. (2000). Cutting Edge: Ectopic Expression of the IL-12 Receptor-β2 in Developing and Committed Th2 Cells Does Not Affect the Production of IL-4 or Induce the Production of IFN-γ. The Journal of Immunology, 164(6), 2861–2865. https://doi.org/10.4049/jimmunol.164.6.2861
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