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Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice
Published on: February 18, 2015
Th17 cells bounce off the fungal wall
1University of Massachusetts Medical School, 364 Plantation Street, LRB317, Worcester, MA 01605, USA. stuart.levitz@umassmed.edu
Cell Host & Microbe
|April 22, 2009
Summary
T helper 17 (Th17) cells are crucial for fighting Candida albicans. Mannan, a fungal cell wall component, stimulates the mannose receptor on immune cells, driving IL-17 production.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- T helper 17 (Th17) cells are critical for host defense against fungal pathogens, particularly Candida albicans.
- Understanding the specific fungal components and host receptors involved in Th17 cell activation is essential for developing targeted immunotherapies.
Purpose of the Study:
- To elucidate the specific fungal cell wall components of Candida albicans that trigger Interleukin-17 (IL-17) production.
- To identify the cognate receptors on human peripheral blood mononuclear cells (PBMCs) responsible for recognizing these fungal components and initiating an IL-17 response.
Main Methods:
- Human peripheral blood mononuclear cells (PBMCs) were stimulated with various components of the Candida albicans cell wall.
- Interleukin-17 (IL-17) production levels were quantified following stimulation.
- The role of specific receptors, including the mannose receptor, in mediating the response was investigated.
Main Results:
- Mannan, a major component of the Candida albicans cell wall, was identified as a potent stimulator of IL-17 production by PBMCs.
- The mannose receptor on PBMCs was found to be the predominant receptor responsible for recognizing mannan and inducing IL-17 secretion.
- This highlights a key interaction in the innate immune response to Candida albicans.
Conclusions:
- Mannan-mannose receptor interaction is a critical pathway for initiating Th17-mediated immunity against Candida albicans.
- Targeting this pathway could offer novel therapeutic strategies for invasive fungal infections.
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