Figure 1.
Immune response against intracellular pathogens.
(A) PRRs of APCs sense pathogens that result in the activation of APCs. (B) This leads to enhanced antigen presentation, upregulation of costimulatory molecules, and secretion of proinflammatory cytokines that promote the activation of T cells. The activated T cells help in elimination of the pathogens. (C) Engagement of costimulatory molecules on APCs by T cells also results in “bidirectional signaling” that activates APCs to restrict the growth of pathogens.
Figure 2.
Pathogens modulate the expression of costimulatory molecules for their survival.
Sensing of pathogens through PRRs triggers the activation of APCs. (A) Costimulatory molecules, which act as the second signal for T-cell activation, are upregulated on infected cells. Persistence of intracellular pathogens modulates the expression of costimulatory molecules, such as downregulation of CD40/CD80/CD86 and upregulation of PDL-1 on infected APCs. Similarly, retarding the exhibition of CD28/CD40L augments PD-1/CTLA-4 on T cells. (B) Interaction of T cells with the infected APCs impairs the function of T cells by inducing anergy, apoptosis, or exhaustion. (C) Lack of T-cell help impedes the activity of APCs, eventually enhancing the survival of pathogens.
Table 1.
Exploitation of costimulatory molecules by intracellular pathogens.