Review Article

New Insights about Treg and Th17 Cells in HIV Infection and Disease Progression

Figure 1

The interaction network between transcriptional factors, cytokines, chemokines, and their receptors in Th17 and Treg cells. The fine-tuning of Th17/Treg balance is regulated by expression of transcription factors that are activated by cytokines milieu and their receptors. TGF-β along with mainly IL-6 induces RORc, ROR-α, or STAT3 expression to differentiate Th17 cells while that in combination with IL-2 induces FoxP3 expression to differentiate Treg cells, while homing and immunological cells recruitment of both cell subsets are powerful mechanism mediated by chemokines and their chemokine receptors such as CCR6, CCR4, or CXCR3 which facilitates the recruitment of suppressive Treg and inflammatory effector Th17 cells (e.g., by means of CCR6-CCL20) into the site infection or injured tissue. Of note, other immunological cells, as dendritic cells, influence this balance because they produce cytokines, chemokines, and other molecules that participate in this interaction network.