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The macrophage mannose receptor induces IL-17 in response to Candida albicans

Frank L van de Veerdonk1, Renoud J Marijnissen, Bart Jan Kullberg

  • 1Department of Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Cell Host & Microbe
|April 22, 2009
PubMed

Insights

This study identifies pattern recognition receptors that trigger T helper 17 (Th17) cell responses during fungal infection. Candida mannan, via the macrophage mannose receptor (MR), initiates Th17 immunity without artificial stimulation.

Area of Science:

  • Immunology
  • Microbiology
  • Infectious Disease

Background:

  • Interleukin-17 (IL-17) is crucial for neutrophil-mediated inflammation.
  • The specific innate immune receptors inducing T helper 17 (Th17) responses during pathogen infection are not fully understood, especially without artificial mitogenic stimulation.

Purpose of the Study:

  • To identify the pattern recognition receptors (PRRs) and pathogen-associated molecular patterns (PAMPs) that trigger Th17 responses during host defense against microbial pathogens.
  • To elucidate the mechanisms underlying Th17 induction by the fungal pathogen Candida albicans.

Main Methods:

  • Investigated innate immune receptors and PAMPs involved in Th17 induction.
  • Utilized Candida albicans as a prototypic fungal pathogen.
  • Assessed IL-17 production in response to various microbial components, including Candida mannan, zymosan, beta-glucans, Toll-like receptor (TLR) agonists, and NOD2 ligand MDP.
  • Determined the role of antigen-presenting cells and the macrophage mannose receptor (MR) in Candida-induced IL-17 responses.
  • Examined the contribution of TLR2, dectin-1, TLR4, and NOD2 pathways in amplifying MR-induced IL-17 production.

Main Results:

  • Candida albicans induced IL-17 production more potently than Gram-negative bacteria.
  • Candida mannan was identified as a potent inducer of IL-17 in the absence of anti-CD3/anti-CD28 stimulation.
  • The Candida-induced IL-17 response was dependent on antigen-presenting cells and the macrophage mannose receptor (MR).
  • The TLR2/dectin-1 pathway amplified MR-induced IL-17 production, while TLR4 and NOD2 did not.
  • Identified specific PRRs triggering Th17 responses during pathogen-specific defense without mitogenic stimuli.

Conclusions:

  • Candida mannan, acting through the macrophage mannose receptor (MR), initiates Th17 responses during Candida albicans infection.
  • The TLR2/dectin-1 pathway plays a role in amplifying this MR-dependent Th17 induction.
  • This study elucidates key innate immune pathways involved in initiating Th17 immunity against fungal pathogens.

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