Summary

Invasive and superficial fungal infections pose a growing global health challenge, especially in individuals with weakened immunity. The host employs a coordinated network of innate and adaptive defences to control fungal invasion. Innate immunity relies on phagocytic cells—macrophages, neutrophils and dendritic cells—that detect cell-wall components such as β-glucans, mannans, chitin and melanin via pattern recognition receptors. Engagement of dectin-1, Toll-like receptors and complement receptors triggers phagocytosis, reactive oxygen species production and secretion of cytokines that shape adaptive responses. Complement activation through classical, lectin and alternative pathways further enhances pathogen elimination by coating fungal surfaces with opsonins. Soluble mediators including collectins and long pentraxins amplify these processes. Adaptive immunity, notably T helper 1 and T helper 17 cells, reinforces clearance through interferon-γ and interleukin-17 production. Many pathogenic fungi evade host defences by masking immunogenic structures, secreting proteases to inactivate complement and modulating cytokine signalling. Understanding these dynamic interactions is essential for developing immunotherapies and vaccines against resistant mycoses.

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Immune Responses to Fungal Pathogens publication trend

The graph below shows the total number of articles in immune responses to fungal pathogens across all publications each year (not limited to Nature Index journals).

Technical terms

Pattern recognition receptor (PRR): A receptor of the innate immune system that detects conserved molecular motifs on pathogens.

Opsonisation: The coating of pathogens with proteins such as antibodies or complement to enhance their uptake by phagocytes.

Pentraxin 3 (PTX3): A soluble pattern recognition molecule that binds microbial surfaces and activates complement.

Lectin pathway: A complement activation route triggered by carbohydrate-binding proteins such as mannose-binding lectin.

Collectin: A family of collagen-containing C-type lectins, including surfactant proteins, that recognise microbial carbohydrates and promote clearance.

References

  1. A Sweet Response to a Sour Situation: The Role of Soluble Pattern Recognition Receptors in the Innate Immune Response to Invasive Aspergillus fumigatus Infections. PLOS Pathogens (2016).
  2. Immune Recognition of Fungal Polysaccharides. Journal of Fungi (2017).
  3. The complement system in Aspergillus fumigatus infections and its crosstalk with pentraxins. FEBS Letters (2020).
  4. Fungal melanin stimulates surfactant protein D–mediated opsonization of and host immune response to Aspergillus fumigatus spores. Journal of Biological Chemistry (2018).
  5. Aspergillus fumigatus conidial metalloprotease Mep1p cleaves host complement proteins. Journal of Biological Chemistry (2018).
  6. Complementary Roles of the Classical and Lectin Complement Pathways in the Defense against Aspergillus fumigatus. Frontiers in Immunology (2016).

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