Research output: Contribution to journal › Article › Academic › peer-review
FcαRI co-stimulation converts human intestinal CD103+ dendritic cells into pro-inflammatory cells through glycolytic reprogramming. / Hansen, Ivo S.; Krabbendam, Lisette; Bernink, Jochem H. et al.
In: Nature communications, Vol. 9, No. 1, 2018, p. 863.Research output: Contribution to journal › Article › Academic › peer-review
}
TY - JOUR
T1 - FcαRI co-stimulation converts human intestinal CD103+ dendritic cells into pro-inflammatory cells through glycolytic reprogramming
AU - Hansen, Ivo S.
AU - Krabbendam, Lisette
AU - Bernink, Jochem H.
AU - Loayza-Puch, Fabricio
AU - Hoepel, Willianne
AU - van Burgsteden, Johan A.
AU - Kuijper, Elsa C.
AU - Buskens, Christianne J.
AU - Bemelman, Willem A.
AU - Zaat, Sebastiaan A. J.
AU - Agami, Reuven
AU - Vidarsson, Gestur
AU - van den Brink, Gijs R.
AU - de Jong, Esther C.
AU - Wildenberg, Manon E.
AU - Baeten, Dominique L. P.
AU - Everts, Bart
AU - den Dunnen, Jeroen
PY - 2018
Y1 - 2018
N2 - +DCs. These cells then enhance inflammation by promoting Th17 responses and activating human intestinal innate lymphoid cells 3. Moreover, FcαRI-induced cytokine production is orchestrated via upregulation of cytokine translation and caspase-1 activation, which is dependent on glycolytic reprogramming mediated by kinases Syk, PI3K and TBK1-IKKε. Our data suggest that the formation of IgA-IC in the human intestine provides an environmental cue for the conversion of a tolerogenic to an inflammatory response
AB - +DCs. These cells then enhance inflammation by promoting Th17 responses and activating human intestinal innate lymphoid cells 3. Moreover, FcαRI-induced cytokine production is orchestrated via upregulation of cytokine translation and caspase-1 activation, which is dependent on glycolytic reprogramming mediated by kinases Syk, PI3K and TBK1-IKKε. Our data suggest that the formation of IgA-IC in the human intestine provides an environmental cue for the conversion of a tolerogenic to an inflammatory response
U2 - 10.1038/s41467-018-03318-5
DO - 10.1038/s41467-018-03318-5
M3 - Article
C2 - 29491406
VL - 9
SP - 863
JO - Nature communications
JF - Nature communications
SN - 2041-1723
IS - 1
ER -
ID: 4637232