Figure 1: Interaction of PRRs and coccidioidal components.
Surface Toll-like receptors (TLRs) as well as other C-type lectins [e.g. Dectin-1 and mannose receptor (MR) and pulmonary surfactant proteins (SP)-A and –D
(SPD)] participate in the recognition of coccidioidal components or PAMPs (e.g.
β-glucan, mannan and other unknown components). In coccidioidal infection,
interaction of fungal PAMPs with PRRs activates a signalling pathway which
occurs at the level of the intracellular adaptor molecule myeloid differentiation
primary-response protein 88 (MyD88). The participations of other adaptor
molecules such as Toll/interleukin-1 receptor (TIR) domain-containing adaptor
protein (TIRAP), MyD88-adaptor-like protein (Mal), TIR domain-containing
adaptor-including interferon-β (TRIF) and transcription factors including nuclear
factor-κB (NF-κB) and interferon regulatory factor (IRF) have not been studied
and remain to be confirmed. TLR-mediated MyD88 signalling and Dectin-1
activation induce the expression of pro-inflammatory cytokines including
TNF-α, MIP-2, IL-6, IL-10 and IL-12, thus driving the immune response.
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