作者
Timothy J. Break,Vasileios Oikonomou,Nicolás Dutzan,Jigar V. Desai,Marc Swidergall,Tilo Freiwald,Daniel Chauss,Oliver J. Harrison,Julie Alejo,D. Williams,Stefania Pittaluga,Chyi‐Chia Richard Lee,Nicolas Bouladoux,Muthulekha Swamydas,Kevin W. Hoffman,Teresa Greenwell‐Wild,Vincent M. Bruno,Lindsey B. Rosen,Wint Lwin,Andy Renteria,Sergio M. Pontejo,James A. Shannon,Ian A. Myles,Peter Olbrich,Elise M. N. Ferré,Monica M. Schmitt,Daniel Martı́n,Daniel L. Barber,Norma V. Solis,Luigi D. Notarangelo,David Serreze,Machiko Matsumoto,Heather D. Hickman,Philip M. Murphy,Mark S. Anderson,Jean K. Lim,Steven M. Holland,Scott G. Filler,Behdad Afzali,Yasmine Belkaid,Niki M. Moutsopoulos,Michail S. Lionakis
摘要
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
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睡觉晒太阳
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