The Th17/Treg Ratio, IL-1RA and sCD14 Levels in Primary HIV Infection Predict the T-cell Activation Set Point in the Absence of Systemic Microbial Translocation
Figure 7
Proposed model of interrelationships between HIV, immune activation and the Th17/Treg ratio.
HIV induces monocyte and T-cell activation either directly (e.g. through TLRs) or indirectly, through innate and adaptive responses. The Th17 to Treg ratio decreases as Tregs expand in HIV infection and Th17 cells are one of the preferential targets of the virus. HIV can induce IDO expression by antigen-presenting cells which leads to tryptophan (Trp) catabolites accumulation that inhibit Th17 cells and induce Tregs. This further accentuates the decrease in the Th17/Treg ratio. In addition, IL-1RA secreted by activated monocytes could inhibit Th17 cell development. Then, in a later phase of infection – and not in acute infection – the loss of Th17 cells might contribute to microbial translocation that participates in chronic immune activation.