Control of TH17 cells occurs in the small intestine.

Enric Esplugues; Samuel Huber; Nicola Gagliani; Anja E Hauser; Terrence Town; Yisong Y Wan; William O'Connor; Anthony Rongvaux; Van Rooijen Nico; Ann M Haberman; Yoichiro Iwakura; Vijay K Kuchroo; Jay K Kolls; Jeffrey A Bluestone; Kevan C Herold; Richard A Flavell

Control of TH17 cells occurs in the small intestine.

Standard

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, Vol. 475, No. 7357, 7357, 2011, p. 514-518.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Esplugues, E, Huber, S , Gagliani, N, Hauser, AE, Town, T, Wan, YY, O'Connor, W, Rongvaux, A, Nico, VR, Haberman, AM, Iwakura, Y, Kuchroo, VK, Kolls, JK, Bluestone, JA, Herold, KC & Flavell, RA 2011, 'Control of TH17 cells occurs in the small intestine.', NATURE, vol. 475, no. 7357, 7357, pp. 514-518. <http://www.ncbi.nlm.nih.gov/pubmed/21765430?dopt=Citation>

APA

Esplugues, E., Huber, S., Gagliani, N., Hauser, A. E., Town, T., Wan, Y. Y., O'Connor, W., Rongvaux, A., Nico, V. R., Haberman, A. M., Iwakura, Y., Kuchroo, V. K., Kolls, J. K., Bluestone, J. A., Herold, K. C., & Flavell, R. A. (2011). Control of TH17 cells occurs in the small intestine. NATURE, 475(7357), 514-518. [7357]. http://www.ncbi.nlm.nih.gov/pubmed/21765430?dopt=Citation

Vancouver

Esplugues E, Huber S , Gagliani N, Hauser AE, Town T, Wan YY et al. Control of TH17 cells occurs in the small intestine. NATURE. 2011;475(7357):514-518. 7357.

Bibtex

@article{871d8d448c5944818e2c3bd020705f28,

title = "Control of TH17 cells occurs in the small intestine.",

abstract = "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.",

keywords = "Animals, Male, Female, Disease Models, Animal, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Gene Expression Profiling, Mice, Transgenic, Cell Movement/drug effects, Antibodies/immunology/pharmacology, Antigens, CD3/immunology, CD4-Positive T-Lymphocytes/immunology/transplantation, Chemokine CCL20/immunology, Encephalomyelitis, Autoimmune, Experimental/immunology, Gene Expression Regulation/immunology, Influenza A virus/immunology, Interleukin-17/immunology, Intestine, Small/cytology/*immunology, Orthomyxoviridae Infections/immunology, Receptors, CCR6/immunology, Sepsis/immunology, Staphylococcal Infections/immunology, Th17 Cells/*immunology, Animals, Male, Female, Disease Models, Animal, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Gene Expression Profiling, Mice, Transgenic, Cell Movement/drug effects, Antibodies/immunology/pharmacology, Antigens, CD3/immunology, CD4-Positive T-Lymphocytes/immunology/transplantation, Chemokine CCL20/immunology, Encephalomyelitis, Autoimmune, Experimental/immunology, Gene Expression Regulation/immunology, Influenza A virus/immunology, Interleukin-17/immunology, Intestine, Small/cytology/*immunology, Orthomyxoviridae Infections/immunology, Receptors, CCR6/immunology, Sepsis/immunology, Staphylococcal Infections/immunology, Th17 Cells/*immunology",

author = "Enric Esplugues and Samuel Huber and Nicola Gagliani and Hauser, {Anja E} and Terrence Town and Wan, {Yisong Y} and William O'Connor and Anthony Rongvaux and Nico, {Van Rooijen} and Haberman, {Ann M} and Yoichiro Iwakura and Kuchroo, {Vijay K} and Kolls, {Jay K} and Bluestone, {Jeffrey A} and Herold, {Kevan C} and Flavell, {Richard A}",

year = "2011",

language = "English",

volume = "475",

pages = "514--518",

journal = "NATURE",

issn = "0028-0836",

publisher = "NATURE PUBLISHING GROUP",

number = "7357",

}

RIS

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