Pneumocystis and interactions with host immune receptors
Fig 1
MSG and β-1,3-glucan are the main surface proteins of PC recognized by the host; however, novel T-cell and B cell epitopes have been described. Soluble CLRs such as SP-A and SP-D influence PC clearance or escape, respectively. Mannose receptor and Dectin-2 have been shown to recognize PC but do not seem to contribute to clearance, shown in gene-deficient mice. In contrast, Dectin-1 and Mincle have been shown to recognize PC and, in immunocompromised mice, contribute to limiting disease progression. Similarly, MyD88 was shown to be involved in the host response in immunocompromised mice, potentially mediated through TLR2. AM, alveolar macrophage; CLR, C-type lectin receptor; FcRy, Fc receptor common gamma-chain; gpA, glycoprotein A; Mincle, Macrophage inducible Ca2+-dependent lectin receptor; MSG, major surface glycoprotein; MyD88, myeloid differentiation primary response 88; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; PC, Pneumocystis; SP, surfactant protein; Syk, Spleen tyrosine kinase; TLR, toll-like receptor [7,10,17,21,26,29,35].