Get access

Minireview: host defence in invasive aspergillosis

Authors


C. Lass-Flörl, Division of Hygiene and Medical Microbiology, Innsbruck Medical University, Fritz-Pregl-Str. 3, 6020 Innsbruck, Austria.
Tel.: +43 512 900370703. Fax: +43 512 900373700.
E-mail: cornelia.lass-floerl@i-med.ac.at

Summary

Aspergillus is a saprophytic fungus, which mainly becomes pathogenic in immunosuppressed hosts. A failure of host defences results in a diverse set of illnesses, ranging from chronic colonisation, aspergilloma, invasive disease and hypersensitivity. A key concept in immune responses to Aspergillus species is that host susceptibility determines the morphological form, antigenic structure and physical location of the fungus. Traditionally, innate immunity has been considered as a first line of defence and activates adaptive immune mechanisms by the provision of specific signals; innate and adaptive immune responses are intimately linked. The T-helper cell (TH1) response is associated with increased production of inflammatory cytokines IFN-γ, IL-2 and IL-12 and stimulation of antifungal effector cells. Alternatively, TH2-type responses are associated with suppression of antifungal effector cell activity, decreased production of IFN-γ and increased concentrations of IL-4 and IL-10, which promote humoral responses to Aspergillus. The host’s defensive capacity is defined by the sum of resistance and tolerance. Resistance displays the ability to limit fungal burden and elimination of the pathogen, and tolerance means the ability to limit host damage caused by immune response.

Get access to the full text of this article

Ancillary