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Published on: June 19, 2013
The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors
Surabhi Goyal1,2, Juan Camilo Castrillón-Betancur2,3, Esther Klaile2
1Institute for Microbiology and Hygiene, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Abstract:
Fungi, usually present as commensals, are a major cause of opportunistic infections in immunocompromised patients. Such infections, if not diagnosed or treated properly, can prove fatal. However, in most cases healthy individuals are able to avert the fungal attacks by mounting proper antifungal immune responses. Among the pattern recognition receptors (PRRs), C-type lectin receptors (CLRs) are the major players in antifungal immunity. CLRs can recognize carbohydrate ligands, such as β-glucans and mannans, which are mainly found on fungal cell surfaces. They induce proinflammatory immune reactions, including phagocytosis, oxidative burst, cytokine, and chemokine production from innate effector cells, as well as activation of adaptive immunity via Th17 responses. CLRs such as Dectin-1, Dectin-2, Mincle, mannose receptor (MR), and DC-SIGN can recognize many disease-causing fungi and also collaborate with each other as well as other PRRs in mounting a fungi-specific immune response. Mutations in these receptors affect the host response and have been linked to a higher risk in contracting fungal infections. This review focuses on how CLRs on various immune cells orchestrate the antifungal response and on the contribution of single nucleotide polymorphisms in these receptors toward the risk of developing such infections.
Insights
C-type lectin receptors (CLRs) are key to antifungal immunity, recognizing fungal components to trigger immune responses. Genetic variations in CLRs increase susceptibility to potentially fatal fungal infections.
Area of Science:
- Immunology
- Mycology
- Genetics
Background:
- Fungi cause opportunistic infections in immunocompromised individuals.
- Healthy individuals typically mount effective antifungal immune responses.
- Pattern recognition receptors (PRRs), especially C-type lectin receptors (CLRs), are crucial for antifungal immunity.
Purpose of the Study:
- To review the role of CLRs in orchestrating antifungal immune responses.
- To examine the contribution of CLR single nucleotide polymorphisms (SNPs) to fungal infection risk.
Main Methods:
- Review of current literature on CLRs and antifungal immunity.
- Analysis of CLR function in recognizing fungal cell surface carbohydrates (e.g., β-glucans, mannans).
- Discussion of CLR-mediated immune reactions (phagocytosis, cytokine production, Th17 activation).
Main Results:
- CLRs like Dectin-1, Dectin-2, Mincle, MR, and DC-SIGN recognize diverse fungi.
- CLRs collaborate with each other and other PRRs for effective antifungal responses.
- Mutations/SNPs in CLRs are linked to increased susceptibility to fungal infections.
Conclusions:
- CLRs are central to innate and adaptive antifungal immunity.
- Understanding CLR function and genetic variations is vital for managing fungal infections.
- Targeting CLRs may offer new therapeutic strategies against fungal diseases.
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