Fig. 1.
Fig. 1. (A) Cytokines controlling the development of cell-mediated (TH1) and humoral (TH2) responses. Certain infections such as viruses induce the production of IL-12 and IFN-γ by antigen presenting cells (APC). These factors promote the differentiation of TH0 cells to the TH1 phenotype. Other infections such as helminths induce the production of IL-4 (by eosinophils) which induces differentiation to the TH2 phenotype. TH1 cytokines such as IFN-γ inhibit the production of IL-4 and IL-10 while TH2 cytokines such as IL-10 inhibit the production and action of IL-12. (Part B) Factors such as IL-12 and IFN-γ activate a cascade of intracellular signaling molecules including molecules in the JAK/STAT pathway. In contrast, inhibitory molecules may produce their inhibitory effects in part via the activation of molecules such as phosphatases in the case of TGF-β, and SOCS genes in the case of IL-10. These pathways would serve to attenuate a biological response.

(A) Cytokines controlling the development of cell-mediated (TH1) and humoral (TH2) responses. Certain infections such as viruses induce the production of IL-12 and IFN-γ by antigen presenting cells (APC). These factors promote the differentiation of TH0 cells to the TH1 phenotype. Other infections such as helminths induce the production of IL-4 (by eosinophils) which induces differentiation to the TH2 phenotype. TH1 cytokines such as IFN-γ inhibit the production of IL-4 and IL-10 while TH2 cytokines such as IL-10 inhibit the production and action of IL-12. (Part B) Factors such as IL-12 and IFN-γ activate a cascade of intracellular signaling molecules including molecules in the JAK/STAT pathway. In contrast, inhibitory molecules may produce their inhibitory effects in part via the activation of molecules such as phosphatases in the case of TGF-β, and SOCS genes in the case of IL-10. These pathways would serve to attenuate a biological response.

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