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Updated: Aug 7, 2026

Live-cell Video Microscopy of Fungal Pathogen Phagocytosis
Published on: January 9, 2013
Candida-host cell receptor-ligand interactions
1St Johns Cardiovascular Research Center, Division of Infectious Diseases, Department of Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA 90502, USA. sfiller@ucla.edu
Abstract:
The interaction of Candida species with their cognate host receptors is a key factor in the pathogenesis of different types of candidiasis. The recognition of different forms of Candida albicans by Toll-like receptors 2 and 4 on mononuclear leukocytes has recently been discovered to determine the function and activity of regulatory T-cells, determine the balance of Type 1 and Type 2 cytokines and, thereby, influence the antifungal activity of both the innate and adaptive immune response. Different forms of C. albicans are also recognized by different lectins that are expressed on the surface macrophages. C. albicans and Candida glabrata express the ALS (agglutinin-like sequence) and EPA (epithelial adhesin) families of adhesins, respectively. A key difference between C. glabrata and C. albicans is that EPA expression in C. glabrata is governed by sub-telomeric silencing, whereas ALS expression in C. albicans is regulated by other mechanisms.
Insights
Host receptor interactions with Candida species are crucial for candidiasis pathogenesis. Recognition by Toll-like receptors and lectins influences immune responses and fungal clearance.
Area of Science:
- Immunology
- Microbiology
- Mycology
Background:
- Candida species interactions with host receptors are central to candidiasis pathogenesis.
- Recognition of Candida albicans by Toll-like receptors (TLRs) 2 and 4 on mononuclear leukocytes impacts regulatory T-cell activity and cytokine balance.
- Macrophages recognize different Candida forms via surface lectins.
Purpose of the Study:
- To elucidate the role of host-pathogen interactions in Candida infections.
- To understand how immune cells recognize and respond to different Candida species.
- To investigate the mechanisms regulating fungal adhesin expression.
Main Methods:
- Analysis of Candida species recognition by host immune cells.
- Investigation of Toll-like receptor and lectin involvement in immune responses.
- Comparison of adhesin gene regulation in Candida albicans and Candida glabrata.
Main Results:
- Candida albicans recognition by TLR2 and TLR4 influences T-cell responses and cytokine profiles, modulating innate and adaptive antifungal immunity.
- Different Candida forms are differentially recognized by macrophage lectins.
- Candida albicans expresses agglutinin-like sequence (ALS) adhesins, while Candida glabrata expresses epithelial adhesin (EPA) adhesins.
- EPA expression in C. glabrata is regulated by sub-telomeric silencing, distinct from ALS regulation in C. albicans.
Conclusions:
- Host receptor interactions are critical determinants of the immune response to Candida infections.
- Differential recognition mechanisms contribute to the varying pathogenesis of candidiasis.
- Distinct regulatory mechanisms for adhesin expression in C. albicans and C. glabrata highlight species-specific adaptations.
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