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Flying under the radar: Histoplasma capsulatum avoidance of innate immune recognition
Stephanie C Ray1, Chad A Rappleye1
1Ohio State University, Columbus, OH, 43210, USA.
Abstract:
The dimorphic fungal pathogen Histoplasma capsulatum takes advantage of the innate immune system, utilizing host macrophages as a proliferative niche while largely avoiding stimulation of signaling host receptors. As a result, innate immune cells are unable to control H. capsulatum on their own. Not all host phagocytes respond to H. capsulatum in the same way, with neutrophils and dendritic cells playing important roles in impeding fungal growth and initiating a protective TH1 response, respectively. Dendritic cells prime T-cell differentiation after internalization of yeasts via VLA-5 receptors and subsequent degradation of the yeasts. Dendritic cell-expressed TLR7 and TLR9 promote a type I interferon response for TH1 polarization. In contrast to dendritic cells, macrophages provide a hospitable intracellular environment. H. capsulatum yeasts enter macrophages via binding to phagocytic receptors. Simultaneously, α-glucan masks immunostimulatory cell wall β-glucans and a secreted endoglucanase removes exposed β-glucans to minimize recognition of yeasts by Dectin-1. This review highlights how phagocytes interact with H. capsulatum yeasts and the mechanisms H. capsulatum uses to limit the innate immune response.
Insights
Histoplasma capsulatum evades innate immunity by using macrophages as a niche and masking its cell wall components. This fungal pathogen limits immune responses, hindering control by phagocytes.
Area of Science:
- Immunology
- Mycology
- Pathogen-Host Interactions
Background:
- Histoplasma capsulatum is a dimorphic fungal pathogen that infects macrophages.
- Innate immune cells struggle to control H. capsulatum due to its immune evasion strategies.
Purpose of the Study:
- To review the interactions between phagocytes and H. capsulatum.
- To highlight the mechanisms H. capsulatum employs to evade the innate immune response.
Main Methods:
- Review of scientific literature on Histoplasma capsulatum and host immune interactions.
- Analysis of fungal cell wall components and their role in immune evasion.
- Examination of phagocyte-specific responses to H. capsulatum.
Main Results:
- Macrophages serve as a proliferative niche for H. capsulatum, while neutrophils and dendritic cells impede fungal growth and initiate TH1 responses.
- Dendritic cells utilize VLA-5 receptors and TLR7/TLR9 to promote TH1 polarization.
- H. capsulatum masks β-glucans with α-glucan and uses endoglucanase to prevent Dectin-1 recognition, thus minimizing immune stimulation.
Conclusions:
- Phagocyte interactions with H. capsulatum are diverse, with distinct roles for macrophages, neutrophils, and dendritic cells.
- H. capsulatum actively manipulates the host immune system to establish infection.
- Understanding these interactions is crucial for developing effective therapeutic strategies against histoplasmosis.
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