Regulatory T cells in paracoccidioidomycosis

Figures & data

Figure 1. Pulmonary paracoccidioidomycosis: influence of PRRs on the expansion of Treg cells and other T cell subsets. This figure summarizes the influence of TLRs, MyD88, CLRs (dectin-1 and MR), and NLRP3 inflammasome in pulmonary PCM. Toll 2 and Toll 4 signaling exert opposing influences on T cell activation. While Toll 4 induces prevalent production of pro-inflammatory T cell subsets and reduces Treg expansion, Toll 2 signaling stimulates the prevalent differentiation of Treg cells and concomitant impairment of Th17 immunity. The adapter molecule MyD88, which controls the signaling of almost all Toll-like receptors and the IL-1 family of receptors, is fundamental to the differentiation of all T cell subsets including Treg cells. Dectin-1 via Syk – CARD9 mediated signaling is also involved in the differentiation of Th17 and Tc17 subsets with concomitant inhibition of Treg cell proliferation. MR is another CLR involved in Th17 differentiation. In pulmonary PCM, NLRP3 inflammasome mediates the prevalent differentiation of Th1 and Th17 cells and impairs Treg cell proliferation. PRRs, pattern recognition receptors; TLR2 and TLR4, Toll-like receptors 2 and 4; MyD88, myeloid differentiation factor 88; CLRs, C-type lectin receptors; MR, mannose receptor; NLRP3, NOD-like receptor P3.