Cracking the Toll-like receptor code in fungal infections

Abstract

Innate control of fungal infection requires the specific recognition of invariant fungal molecular structures by a variety of innate immune receptors, including Toll-like receptors. In addition to the role in inducing protective immune responses, Toll-like receptor engagement may paradoxically favor fungal infections, by inducing inflammatory pathology and impairing antifungal immunity. Although the dissection of complex genetic traits modulating susceptibility to fungal infections is complex, the contribution of host genetics may hold the key to elucidating new risk factors for these severe, often fatal diseases. Understanding host–pathogen interactions at the innate immune interface will eventually lead to the development of new therapeutics and genetic markers in fungal infections.

Keywords::

• fungal infections
• genetic susceptibility
• inflammation
• innate immunity
• Toll-like receptors

Acknowledgements

The authors thank Cristina Massi Benedetti for digital art and editing.

Financial & competing interests disclosure

This work was supported by the Specific Targeted Research Projects SYBARIS (FP7-HEALTH-2009), contract number 242220, and by the Italian Project PRIN 2007KLCKP8_004. Cristina Cunha and Agostinho Carvalho were financially supported by fellowships from Fundação para a Ciência e Tecnologia, Portugal (contracts SFRH/BD/65962/2009 and SFRH/BPD/46292/2008, respectively). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Notes

TLR: Toll-like receptor.