Control of TH17 cells occurs in the small intestine.
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Control of TH17 cells occurs in the small intestine. / Esplugues, Enric; Huber, Samuel; Gagliani, Nicola; Hauser, Anja E; Town, Terrence; Wan, Yisong Y; O'Connor, William; Rongvaux, Anthony; Nico, Van Rooijen; Haberman, Ann M; Iwakura, Yoichiro; Kuchroo, Vijay K; Kolls, Jay K; Bluestone, Jeffrey A; Herold, Kevan C; Flavell, Richard A.
in: NATURE, Jahrgang 475, Nr. 7357, 7357, 2011, S. 514-518.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Control of TH17 cells occurs in the small intestine.
AU - Esplugues, Enric
AU - Huber, Samuel
AU - Gagliani, Nicola
AU - Hauser, Anja E
AU - Town, Terrence
AU - Wan, Yisong Y
AU - O'Connor, William
AU - Rongvaux, Anthony
AU - Nico, Van Rooijen
AU - Haberman, Ann M
AU - Iwakura, Yoichiro
AU - Kuchroo, Vijay K
AU - Kolls, Jay K
AU - Bluestone, Jeffrey A
AU - Herold, Kevan C
AU - Flavell, Richard A
PY - 2011
Y1 - 2011
N2 - Interleukin (IL)-17-producing T helper cells (T(H)17) are a recently identified CD4(+) T cell subset distinct from T helper type 1 (T(H)1) and T helper type 2 (T(H)2) cells. T(H)17 cells can drive antigen-specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE), the mouse model for multiple sclerosis. The factors that are needed for the generation of T(H)17 cells have been well characterized. However, where and how the immune system controls T(H)17 cells in vivo remains unclear. Here, by using a model of tolerance induced by CD3-specific antibody, a model of sepsis and influenza A viral infection (H1N1), we show that pro-inflammatory T(H)17 cells can be redirected to and controlled in the small intestine. T(H)17-specific IL-17A secretion induced expression of the chemokine CCL20 in the small intestine, facilitating the migration of these cells specifically to the small intestine via the CCR6/CCL20 axis. Moreover, we found that T(H)17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen; second, pro-inflammatory T(H)17 cells simultaneously acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rT(H)17). These results identify mechanisms limiting T(H)17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of T(H)17 cells.
AB - Interleukin (IL)-17-producing T helper cells (T(H)17) are a recently identified CD4(+) T cell subset distinct from T helper type 1 (T(H)1) and T helper type 2 (T(H)2) cells. T(H)17 cells can drive antigen-specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE), the mouse model for multiple sclerosis. The factors that are needed for the generation of T(H)17 cells have been well characterized. However, where and how the immune system controls T(H)17 cells in vivo remains unclear. Here, by using a model of tolerance induced by CD3-specific antibody, a model of sepsis and influenza A viral infection (H1N1), we show that pro-inflammatory T(H)17 cells can be redirected to and controlled in the small intestine. T(H)17-specific IL-17A secretion induced expression of the chemokine CCL20 in the small intestine, facilitating the migration of these cells specifically to the small intestine via the CCR6/CCL20 axis. Moreover, we found that T(H)17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen; second, pro-inflammatory T(H)17 cells simultaneously acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rT(H)17). These results identify mechanisms limiting T(H)17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of T(H)17 cells.
KW - Animals
KW - Male
KW - Female
KW - Disease Models, Animal
KW - Mice
KW - Mice, Inbred BALB C
KW - Mice, Inbred C57BL
KW - Gene Expression Profiling
KW - Mice, Transgenic
KW - Cell Movement/drug effects
KW - Antibodies/immunology/pharmacology
KW - Antigens, CD3/immunology
KW - CD4-Positive T-Lymphocytes/immunology/transplantation
KW - Chemokine CCL20/immunology
KW - Encephalomyelitis, Autoimmune, Experimental/immunology
KW - Gene Expression Regulation/immunology
KW - Influenza A virus/immunology
KW - Interleukin-17/immunology
KW - Intestine, Small/cytology/immunology
KW - Orthomyxoviridae Infections/immunology
KW - Receptors, CCR6/immunology
KW - Sepsis/immunology
KW - Staphylococcal Infections/immunology
KW - Th17 Cells/immunology
KW - Animals
KW - Male
KW - Female
KW - Disease Models, Animal
KW - Mice
KW - Mice, Inbred BALB C
KW - Mice, Inbred C57BL
KW - Gene Expression Profiling
KW - Mice, Transgenic
KW - Cell Movement/drug effects
KW - Antibodies/immunology/pharmacology
KW - Antigens, CD3/immunology
KW - CD4-Positive T-Lymphocytes/immunology/transplantation
KW - Chemokine CCL20/immunology
KW - Encephalomyelitis, Autoimmune, Experimental/immunology
KW - Gene Expression Regulation/immunology
KW - Influenza A virus/immunology
KW - Interleukin-17/immunology
KW - Intestine, Small/cytology/immunology
KW - Orthomyxoviridae Infections/immunology
KW - Receptors, CCR6/immunology
KW - Sepsis/immunology
KW - Staphylococcal Infections/immunology
KW - Th17 Cells/immunology
M3 - SCORING: Journal article
VL - 475
SP - 514
EP - 518
JO - NATURE
JF - NATURE
SN - 0028-0836
IS - 7357
M1 - 7357
ER -