TH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine
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TH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine. / Pascual-Reguant, A; Bayat Sarmadi, J; Baumann, Claudia; Noster, R; Cirera-Salinas, D; Curato, C; Pelczar, P; Huber, S; Zielinski, C E; Löhning, M; Hauser, Anja E; Esplugues, Enric.
in: MUCOSAL IMMUNOL, Jahrgang 10, Nr. 6, 10.2017, S. 1431-1442.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - TH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine
AU - Pascual-Reguant, A
AU - Bayat Sarmadi, J
AU - Baumann, Claudia
AU - Noster, R
AU - Cirera-Salinas, D
AU - Curato, C
AU - Pelczar, P
AU - Huber, S
AU - Zielinski, C E
AU - Löhning, M
AU - Hauser, Anja E
AU - Esplugues, Enric
PY - 2017/10
Y1 - 2017/10
N2 - TH17 cells are major drivers of inflammation and involved in several autoimmune diseases. Tissue inflammation is a beneficial host response to infection, but it can also contribute to autoimmunity. The crosstalk between a tissue and the immune system during an inflammatory response is key for preserving tissue integrity and restoring physiological processes. However, how the inflamed tissue regulates the magnitude of an immune response by controlling pro-inflammatory T cells is not well characterized so far. Here we show that TH17 cells accumulating in the small intestine upon inflammation express the IL-33 receptor (ST2) and intestinal epithelial cells (IEC) are the main source of the alarmin interleukin-33 (IL-33). We show that pro-inflammatory TH17 cells acquire a regulatory phenotype with immunosuppressive properties in response to IL-33. Absence of ST2 signaling promotes the secretion of pro-inflammatory cytokines by TH17 cells and dampens the secretion of IL-10. Our results provide new insights into the mechanisms by which IEC, via IL-33/ST2 axis, may control pro-inflammatory TH17 cells in the small intestine to sustain homeostasis.Mucosal Immunology advance online publication 15 February 2017. doi:10.1038/mi.2017.5.
AB - TH17 cells are major drivers of inflammation and involved in several autoimmune diseases. Tissue inflammation is a beneficial host response to infection, but it can also contribute to autoimmunity. The crosstalk between a tissue and the immune system during an inflammatory response is key for preserving tissue integrity and restoring physiological processes. However, how the inflamed tissue regulates the magnitude of an immune response by controlling pro-inflammatory T cells is not well characterized so far. Here we show that TH17 cells accumulating in the small intestine upon inflammation express the IL-33 receptor (ST2) and intestinal epithelial cells (IEC) are the main source of the alarmin interleukin-33 (IL-33). We show that pro-inflammatory TH17 cells acquire a regulatory phenotype with immunosuppressive properties in response to IL-33. Absence of ST2 signaling promotes the secretion of pro-inflammatory cytokines by TH17 cells and dampens the secretion of IL-10. Our results provide new insights into the mechanisms by which IEC, via IL-33/ST2 axis, may control pro-inflammatory TH17 cells in the small intestine to sustain homeostasis.Mucosal Immunology advance online publication 15 February 2017. doi:10.1038/mi.2017.5.
KW - Journal Article
U2 - 10.1038/mi.2017.5
DO - 10.1038/mi.2017.5
M3 - SCORING: Journal article
C2 - 28198366
VL - 10
SP - 1431
EP - 1442
JO - MUCOSAL IMMUNOL
JF - MUCOSAL IMMUNOL
SN - 1933-0219
IS - 6
ER -
