Cutting edge: ectopic expression of the IL-12 receptor-beta 2 in developing and committed Th2 cells does not affect the production of IL-4 or induce the production of IFN-gamma.

Important note: Information in this article was accurate in 2000. The state of the art may have changed since the publication date.

Cutting edge: ectopic expression of the IL-12 receptor-beta 2 in developing and committed Th2 cells does not affect the production of IL-4 or induce the production of IFN-gamma.

J Immunol. 2000 Mar 15;164(6):2861-5. Unique Identifier : AIDSLINE MED/20171480
Heath VL; Showe L; Crain C; Barrat FJ; Trinchieri G; O'Garra A; Department of Immunobiology, DNAX Research Institute, Palo Alto,; CA 94304, USA. Heath@DNAX.org

Abstract: The IL-12 receptor-beta 2 (IL-12R beta 2) 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-gamma on restimulation in the presence of IL-12. In this study, we ectopically expressed the IL-12 receptor-beta 2 (IL-12R beta 2) bicistronically with enhanced green fluorescent protein by retroviral infection in developing and committed Th2 cells. Restimulation of Th2 cells expressing this ectopic IL-12R beta 2 in the presence of IL-12 led to levels of IL-4 production similar to those in control Th2 cells. The expression of IL-12R beta 2 in Th2 cells did not lead to significant levels of IFN-gamma production, although IL-12-mediated STAT signaling and proliferation were restored. Thus, although the IL-12R beta 2 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.

Keywords: JOURNAL ARTICLE Animal Cell Differentiation/IMMUNOLOGY Cells, Cultured Down-Regulation (Physiology)/IMMUNOLOGY DNA-Binding Proteins/PHYSIOLOGY Immunity, Cellular Immunophenotyping Interferon Type II/*BIOSYNTHESIS Interleukin-12/*METABOLISM/PHYSIOLOGY Interleukin-4/ANTAGONISTS & INHIB/*BIOSYNTHESIS Mice Mice, Transgenic Receptors, Interleukin/*BIOSYNTHESIS Signal Transduction/IMMUNOLOGY Support, Non-U.S. Gov't Th1 Cells/IMMUNOLOGY/METABOLISM Th2 Cells/CYTOLOGY/IMMUNOLOGY/*METABOLISM Trans-Activators/PHYSIOLOGY

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