Abstract
Pneumocystis jirovecii is one of the most common fungal pathogens in immunocompromised individuals. Pneumocystis jirovecii pneumonia (PJP) causes a significant host immune response that is driven greatly by the organism’s cell wall components including β-glucans and major surface glycoprotein (Msg). These ligands interact with a number of C-type lectin receptors (CLRs) leading to downstream activation of proinflammatory signaling pathways. This minireview provides a brief overview summarizing known CLR/Pneumocystis interactions.
Highlights
Pneumocystis jirovecii is the opportunistic fungal organism responsible for Pneumocystis jirovecii pneumonia (PJP) that causes severe morbidity and mortality in immunocompromised individuals and is one of the top 10 severe fungal infections in the world [1]
Surfactant protein A (SP-A), was the first pulmonary surfactant proteins associated with binding to Pneumocystis, with purified SP-A being shown to bind to the mannose rich major surface glycoprotein (Msg) component of the organism [53]
Analyzing the various states of this collectin, we found that higher dodecameric forms of the protein bound fungal organisms significantly greater than the trimeric configuration of the protein [57]
Summary
Received: 19 October 2021 Accepted: 30 November 2021 Published: 16 December 2021. C-Type Lectin Receptors in Pneumocystis Innate Immunity. Pneumocystis jirovecii is one of the most common fungal pathogens in immunocompromised individuals. Pneumocystis jirovecii pneumonia (PJP) causes a significant host immune response that is driven greatly by the organism’s cell wall components including b-glucans and major surface glycoprotein (Msg). These ligands interact with a number of C-type lectin receptors (CLRs) leading to downstream activation of proinflammatory signaling pathways. This minireview provides a brief overview summarizing known CLR/ Pneumocystis interactions
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