Fungal pathogenesis

Copy and cut to evade host defence

Progressive, systemic fungal infections are associated with host immune dysregulation; however, how fungi impair host immune responses is unclear. Sterkel et al. now report that the fungal serine protease di-peptidlyl peptidase IVA (DppIVA) inhibits leukocyte recruitment, differentiation and activation at sites of inflammation in a mouse model of pulmonary infection with Blastomyces dermatitidis. Importantly, they showed that DppIVA mimics the host ectopeptidase CD26 by cleaving CC chemokines and granulocyte–macrophage-colony stimulating factor (GM-CSF) to evade host defences. In agreement with this, decreasing the expression of fungal DppIVA or treatment with selective DppIVA inhibitors restored leukocyte recruitment and function, and control of disease. These data establish the fungal virulence factor DppIVA as a potential therapeutic drug target.


  1. 1

    Sterkel, A. K. et al. Fungal mimicry of a mammalian aminopeptidase disables innate immunity and promotes pathogenicity. Cell Host Microbe (2016)

Download references


Rights and permissions

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Du Toit, A. Copy and cut to evade host defence. Nat Rev Microbiol 14, 193 (2016).

Download citation


Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing