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Evidence of Positive Cross-Regulation on Th1 by Th2 and Antigen-Presenting Cells: Effects on Th1 Induced by IL-4 and IL-12¹

Timothy B. Oriss^*,, Susan A. McCarthy^*,,§, Martha A. K. Campana^* and Penelope A. Morel^2,*,,§

^* University of Pittsburgh Cancer Institute, and Departments of Medicine, Surgery, and ^§ Molecular Genetics and Biochemistry, University of Pittsburgh, Pittsburgh, PA 15213

The response of Th cells to cytokines is normally strictly regulated, such that following antigenic stimulation, Th cells respond for only a short period of time, after which they become refractory to cytokine-mediated effects. IL-12, a costimulator of Th1 having no proliferation-inducing capacity of its own, allows Th1 clones and lines to respond to IL-4 when they would otherwise be unable to respond to this cytokine. Cells that have proliferated in response to IL-4 plus IL-12 are fully able to be subsequently activated by specific Ag and APC. Additionally, the response to IL-4 of Th1 effector cells derived from normal murine spleen is enhanced significantly by IL-12. Furthermore, in the presence of IL-12, stimulated Th2 can induce proliferation of Th1 via IL-4 production, in a dual chamber culture system. We hypothesize that the effects of IL-4 and IL-12 represent a novel, positive cross-regulatory pathway that acts on Th1, and is mediated by Th2 (the IL-4 source) and APC (the IL-12 source). We propose this as a way for a Th2 immune response to positively influence an ongoing or waning Th1 response.

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