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Publication : Aberrant type 1 immunity drives susceptibility to mucosal fungal infections.

First Author	Break TJ	Year	2021
Journal	Science	Volume	371
Issue	6526	PubMed ID	33446526
Mgi Jnum	J:300010	Mgi Id	MGI:6501612
Doi	10.1126/science.aay5731	Citation	Break TJ, et al. (2021) Aberrant type 1 immunity drives susceptibility to mucosal fungal infections. Science 371(6526)

abstractText

Human monogenic disorders have revealed the critical contribution of type 17 responses in mucosal fungal surveillance. We unexpectedly found that in certain settings, enhanced type 1 immunity rather than defective type 17 responses can promote mucosal fungal infection susceptibility. Notably, in mice and humans with AIRE deficiency, an autoimmune disease characterized by selective susceptibility to mucosal but not systemic fungal infection, mucosal type 17 responses are intact while type 1 responses are exacerbated. These responses promote aberrant interferon-gamma (IFN-gamma)- and signal transducer and activator of transcription 1 (STAT1)-dependent epithelial barrier defects as well as mucosal fungal infection susceptibility. Concordantly, genetic and pharmacologic inhibition of IFN-gamma or Janus kinase (JAK)-STAT signaling ameliorates mucosal fungal disease. Thus, we identify aberrant T cell-dependent, type 1 mucosal inflammation as a critical tissue-specific pathogenic mechanism that promotes mucosal fungal infection susceptibility in mice and humans.

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43 Authors

Lionakis MS,
Dutzan N,
Solis NV,
Serreze DV,
Murphy PM,
Swamydas M,
Martin D,
Genomics and Computational Biology Core,
Belkaid Y,
Anderson MS,
Break TJ,
Renteria A,
Oikonomou V,
Freiwald T,
Lim JK,
Hoffman KW,
Barber DL,
Hickman HD,
Lwin W,
Williams DW,
Schmitt M,
Holland SM,
Notarangelo LD,
Greenwell-Wild T,
Alejo J,
Moutsopoulos NM,
Harrison OJ,
Rosen LB,
Filler SG,
Pittaluga S,
Olbrich P,
Bruno VM,
Chauss D,
Shannon JP,
Bouladoux N,
Lee CR,
Myles IA,
Desai JV,
Ferr? EMN,
Matsumoto M,
Swidergall M,
Pontejo SM,
Afzali B

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