Microorganisms killing by dendritic cells (DCs) is an important effector mechanism during innate immune response, as it can avoid dissemination of infection during migration of these cells toward draining lymph nodes. However, this function depends on pattern recognition receptors (PRRs) to which the microorganism will bind in these cells. Regarding this, TLR9 activation, by stimulating the oxidative metabolism, induces increase in microbicidal activity of these cells. Accordingly, we showed that DCs treatment with a TLR9 agonist results in an increase in fungicidal activity of these cells against the fungus Paracoccidioides brasiliensis (Pb), which however, was not associated to higher H2O2 levels.
Paracoccidioidomycosis (PCM) is a systemic mycosis, endemic to most Latin American countries (especially Brazil) whose etiologic agent is the thermodimorphic fungus Paracoccidioides brasiliensis (Pb). Host resistance/susceptibility to PCM has been explained by the involvement of different subpopulations of CD4 + cells. However, the mechanisms leading to preferential induction of any subpopulation are still unclear, and the participation of dendritic cells (DCs) must be highlighted. These cells bind, capture, kill, process microorganisms and migrate to peripheral lymphoid tissue where they maturate, efficiently trigger, and drive CD4 + T cell-mediated immune responses. The nature of the interaction of these cells with each microorganism defines CD4 + cell differentiation. Few studies have evaluated which subsets of CD4+ cells are preferentially induced after the interaction of human DCs/Pb. Here, we show that in vitro challenge of DCs with Pb results in the preferential induction of T reg cells.
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