IFN-γ Priming Effects on the Maintenance of Effector Memory CD4⁺ T Cells and on Phagocyte Function: Evidences from Infectious Diseases

Figure 1

Schematic illustration to explain the IFN-γ priming effects on APCs and / cells during chronic infections. This figure explains how IFN-γ produced by cells act on APCs (usually DCs) and directly on CD4⁺ T cells during chronic infections. (a) When the pathogen is still present, antigen- (Ag-) bearing APCs activate CD4⁺ T cells that produce small amounts of IFN-γ. These small amounts of IFN-γ are enough to maintain APCs poised for function, for example, phagocytosis, cytokine production, and antigen presentation. At the same time, IFN-γ acts directly on CD4⁺ T cells and maintains the pool of / cells. Both effects culminate in enhanced immune system activation, cytokine production, and pathogen clearance. (b) After complete pathogen elimination, the IFN-γ priming on APCs and / cells ceases and, in consequence, these effector populations rapidly decline. The remaining cells are important to control a secondary infection. However, in some infectious diseases such as malaria, continuous IFN-γ priming, and persistence of / cells seem to be required to protect against reinfection.

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