Feng X., Andersson T., Gschwend J., Flüchter P., Berest I.,Muff J.L., Carchidi D., Lechner A., de Tenorio J.C., Brander N., Boehm U., Klose Ch. S.N., Artis D., Leinder-Zufall T., Zufall F., Schneider Ch.
Tuft cell IL-17RB restrains IL-25 bioavailability and reveals context-dependent ILC2 hypoproliferation
bioRxiv. March 8, 2024
Gschwend J., Sherman S., Ridder F., Feng X., Liang H.E., Locksley R.M., Becher B., Schneider Ch.
Alveolar macrophages rely on GM-CSF from alveolar epithelial type 2 cells before and after birth.
J Exp Med. October 4, 2021
E O'Leary C. , Feng X., Cortez V.C., Locksley R.M., Schneider Ch.
Interrogating the Small Intestine Tuft Cell-ILC2 Circuit Using In Vivo Manipulations
Curr Protoc. March 1, 2021
Ricardo-Gonzalez R.R., Schneider Ch., Liao C., Lee J., Liang H.E., Locksley R.M.
Tissue-specific pathways extrude activated ILC2s to disseminate type 2 immunity.
J Exp Med. April 6, 2020
Schneider Ch., Lee J., Koga S., Ricardo-Gonzales R.R., Nussbaum J.C., Liang H.E., Smith L.K., Villeda S.A., Locksley R.M.
Tissue-resident group 2 innate lymphoid cells differentiate by layered ontogeny and in situ perinatal priming.
Immunity. May 22, 2019
Schneider Ch., O’Leary C.E., von Moltke J., Liang H.E., Ang Q.Y., Turnbaugh P.J., Radhakrishnan S., Pellizzon M., Ma A., Locksley R.M.
A metabolite-triggered tuft cell-ILC2 circuit drives small intestinal remodeling.
Cell. July 12, 2018
Schneider Ch., Nobs S.P., Heer A.K., Hirsch E., Penninger J., Siggs O.M., Kopf M.
Coincidental null mutation of Csf2ra in a colony of PI3Kγ-/- mice causes alveolar macrophage deficiency and fatal respiratory viral infection.
Journal of Leukocyte Biology. July 28, 2016
Schneider Ch., Nobs S.P., Kurrer M., Rehrauer H., Thiele C., Kopf M.
Induction of the nuclear receptor PPAR-γ by the cytokine GM-CSF is critical for the differentiation of fetal monocytes into alveolar macrophages.
Nature Immunology. September 28, 2014
Schneider Ch., Nobs S.P., Heer A., Kurrer M., Klinke G., van Rooijen N., Vogel J., Kopf M.
Alveolar macrophages are essential for protection from respiratory failure and associated morbidity following influenza virus infection.
PLoS Pathogens. April 3, 2014
