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Figure 6 | Malaria Journal

Figure 6

From: Human immune responses to Plasmodium falciparum infection: molecular evidence for a suboptimal THαβ and TH17 bias over ideal and effective traditional TH1 immune response

Figure 6

Proposed model for the four types of host immune response. Green means unchanged and red means up-regulated genes after malaria infection. TH2 immune response is induced by STAT6 activated by IL-4. THαβ immune response is induced by STAT1 & STAT3α activated by IFN-αβ. TH1 immune response is induced by STAT4 activated by IL-12. TH17 immune response is induced by STAT3β activated by TGF-β/IL-6 to induce downstream PMN related genes and pro-inflammatory cytokines (TNFα, IL1, IL8). In THαβ immune response, IFN-α/β can suppress STAT6. IFN-α/β also suppress iNOS and IL-12 via IL-10 dependent mechanism. Up-regulated STAT1 can suppress GATA3 and STAT4. STAT1 can up-regulate IRF1, T-bet, IgG Fc receptors, Fas, C3a receptor. IRF1 induced TRAIL, T-bet induced NK cell killer receptors, and Fas can enhance NK cell cytotoxicity. Up-regulated IgG Fc receptors can mediate ADCC. In T cell, T-bet can up-regulate IFN-γ. Up-regulated IFN-γ can activate STAT1 signalling via IFN-γ receptor. However, the IFN-γ receptor is suppressed during lymphocyte maturation. Thus, THαβ immune response can be separated from TH1 immune response.

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