The Experts below are selected from a list of 22827 Experts worldwide ranked by ideXlab platform
Enric Esplugues - One of the best experts on this subject based on the ideXlab platform.
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control of th17 cells occurs in the small intestine
Nature, 2011Co-Authors: Terrence Town, Enric Esplugues, Anja E. Hauser, Nicola Gagliani, Samuel Huber, William OconnorAbstract:Interleukin-17-producing T helper (TH17) cells serve an important role in the immune system, but are strongly implicated in the pathogenesis of numerous autoimmune diseases including rheumatoid arthritis and multiple sclerosis. How the immune system controls TH17 cells in vivo remains unclear. Using mice in which tolerance was induced by CD3-specific antibody, a model of sepsis and influenza A viral infection, Esplugues et al. demonstrate that TH17 cells are kept in check by redirecting the cells to the small intestine where they are eliminated or re-programmed to acquire immunosuppressive and regulatory properties. This work identifies the gastrointestinal tract as a site for control of TH17 cells. Interleukin (IL)-17-producing T helper cells (TH17) are a recently identified CD4+ T cell subset distinct from T helper type 1 (TH1) and T helper type 2 (TH2) cells1. TH17 cells can drive antigen-specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE)2, the mouse model for multiple sclerosis. The factors that are needed for the generation of TH17 cells have been well characterized3,4,5,6. However, where and how the immune system controls TH17 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 TH17 cells can be redirected to and controlled in the small intestine. TH17-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 TH17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen; second, pro-inflammatory TH17 cells simultaneously acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rTH17). These results identify mechanisms limiting TH17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of TH17 cells.
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control of th17 cells occurs in the small intestine
Nature, 2011Co-Authors: Terrence Town, Enric Esplugues, Anja E. Hauser, Nicola Gagliani, Samuel Huber, Yisong Y WanAbstract: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.
Terrence Town - One of the best experts on this subject based on the ideXlab platform.
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control of th17 cells occurs in the small intestine
Nature, 2011Co-Authors: Terrence Town, Enric Esplugues, Anja E. Hauser, Nicola Gagliani, Samuel Huber, William OconnorAbstract:Interleukin-17-producing T helper (TH17) cells serve an important role in the immune system, but are strongly implicated in the pathogenesis of numerous autoimmune diseases including rheumatoid arthritis and multiple sclerosis. How the immune system controls TH17 cells in vivo remains unclear. Using mice in which tolerance was induced by CD3-specific antibody, a model of sepsis and influenza A viral infection, Esplugues et al. demonstrate that TH17 cells are kept in check by redirecting the cells to the small intestine where they are eliminated or re-programmed to acquire immunosuppressive and regulatory properties. This work identifies the gastrointestinal tract as a site for control of TH17 cells. Interleukin (IL)-17-producing T helper cells (TH17) are a recently identified CD4+ T cell subset distinct from T helper type 1 (TH1) and T helper type 2 (TH2) cells1. TH17 cells can drive antigen-specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE)2, the mouse model for multiple sclerosis. The factors that are needed for the generation of TH17 cells have been well characterized3,4,5,6. However, where and how the immune system controls TH17 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 TH17 cells can be redirected to and controlled in the small intestine. TH17-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 TH17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen; second, pro-inflammatory TH17 cells simultaneously acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rTH17). These results identify mechanisms limiting TH17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of TH17 cells.
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control of th17 cells occurs in the small intestine
Nature, 2011Co-Authors: Terrence Town, Enric Esplugues, Anja E. Hauser, Nicola Gagliani, Samuel Huber, Yisong Y WanAbstract: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.
Samuel Huber - One of the best experts on this subject based on the ideXlab platform.
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control of th17 cells occurs in the small intestine
Nature, 2011Co-Authors: Terrence Town, Enric Esplugues, Anja E. Hauser, Nicola Gagliani, Samuel Huber, William OconnorAbstract:Interleukin-17-producing T helper (TH17) cells serve an important role in the immune system, but are strongly implicated in the pathogenesis of numerous autoimmune diseases including rheumatoid arthritis and multiple sclerosis. How the immune system controls TH17 cells in vivo remains unclear. Using mice in which tolerance was induced by CD3-specific antibody, a model of sepsis and influenza A viral infection, Esplugues et al. demonstrate that TH17 cells are kept in check by redirecting the cells to the small intestine where they are eliminated or re-programmed to acquire immunosuppressive and regulatory properties. This work identifies the gastrointestinal tract as a site for control of TH17 cells. Interleukin (IL)-17-producing T helper cells (TH17) are a recently identified CD4+ T cell subset distinct from T helper type 1 (TH1) and T helper type 2 (TH2) cells1. TH17 cells can drive antigen-specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE)2, the mouse model for multiple sclerosis. The factors that are needed for the generation of TH17 cells have been well characterized3,4,5,6. However, where and how the immune system controls TH17 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 TH17 cells can be redirected to and controlled in the small intestine. TH17-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 TH17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen; second, pro-inflammatory TH17 cells simultaneously acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rTH17). These results identify mechanisms limiting TH17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of TH17 cells.
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control of th17 cells occurs in the small intestine
Nature, 2011Co-Authors: Terrence Town, Enric Esplugues, Anja E. Hauser, Nicola Gagliani, Samuel Huber, Yisong Y WanAbstract: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.
Pirus Ghadjar - One of the best experts on this subject based on the ideXlab platform.
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ccr6 CCL20 Chemokine expression profile in distinct colorectal malignancies
Scandinavian Journal of Immunology, 2013Co-Authors: V O Frick, Pirus Ghadjar, C Rubie, K Kolsch, M Wagner, S Graeber, M GlanemannAbstract:Originally, Chemokines and their G-protein-coupled receptors were described to regulate multiple physiological functions, particularly tissue architecture and compartment-specific migration of white blood cells. Now, it is established that the Chemokine/Chemokine receptor system is also used by cancer cells for migration and metastatic spread. Here, we examined the relative levels of CC-Chemokine CCL20 and its corresponding receptor CCR6 in resection specimens from patients with different malignant and non-malignant colorectal diseases as well as in colorectal liver metastases (CRLM). CCL20/CCR6 mRNA and protein expression profiles were assessed by quantitative real-time PCR (qRT-PCR), enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (IHC) in resection specimens from patients with ulcerative colitis (UC, n = 15), colorectal adenoma (CRA, n = 15), colorectal adenocarcinoma (CRC, n = 61) and colorectal liver metastases (CRLM, n = 16). Corresponding non-diseased tissues served as control. In contrast to UC tissues, the CCL20/CCR6 system showed a distinct upregulation in CRA, CRC and CRLM related to corresponding non-affected tissues (P < 0.05, respectively). Furthermore, CRA, CRC and CRLM tissue samples displayed significantly higher protein amounts of CCL20 in comparison with UC specimens (P < 0.05, respectively). Our results strongly suggest an association between CCL20/CCR6 expression and the induction of CRA, CRC and the development of CRLM. Therefore, CCL20 and CCR6 may provide potential targets for novel treatment strategies of CRC.
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miR-21 functionally interacts with the 3'UTR of Chemokine CCL20 and down-regulates CCL20 expression in miR-21 transfected colorectal cancer cells.
Cancer letters, 2011Co-Authors: Benjamin Vicinus, Claudia Rubie, Sabrina K. Faust, Vilma Oliveira Frick, Pirus Ghadjar, Mathias Wagner, Stefan Graeber, Martin K. SchillingAbstract:As deregulation of miRNAs and Chemokine CCL20 was shown to play a role in colorectal cancer (CRC) pathogenesis, we analyzed the functional interactions of candidate miRNAs with CCL20 mRNA. After target prediction software programs indicated a role for miR-21 in CCL20 regulation, we applied the luciferase reporter assay system to demonstrate that miR-21 functionally interacts with the 3'UTR of CCL20 mRNA and down-regulates CCL20 in miR-21 mimic transfected CRC cell lines (Caco-2, SW480 and SW620). Thus, regulation of CCL20 expression by miR-21 might be a regulatory mechanism involved in progression of CRC.
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the Chemokine CCL20 and its receptor ccr6 in human malignancy with focus on colorectal cancer
International Journal of Cancer, 2009Co-Authors: Pirus Ghadjar, Claudia Rubie, Daniel M Aebersold, Ulrich KeilholzAbstract:Chemokines are a superfamily of small chemotactic cytokines, which interact with their G-protein-coupled receptors. These interactions regulate multiple physiological functions, particularly tissue architecture and compartment-specific migration of white blood cells. It has been found that the Chemokine/Chemokine receptor system has been utilized by cancer cells for migration and metastasis. The Chemokine receptor CCR6 is expressed in colorectal cancer and several other cancer types, and stimulation by its physiological Chemokine ligand CCL20 has been reported to promote cancer cell proliferation and migration in vitro. Moreover, CCR6/CCL20 interactions apparently play a role in organ selective liver metastasis of colorectal cancer. Here, we review the literature on expression patterns of CCL20 and CCR6 and their physiological interactions as well as the currently presumed role of CCR6 and CCL20 in the formation of colorectal cancer liver metastasis, providing a potential basis for novel treatment strategies.
Pi Nyvall Collen - One of the best experts on this subject based on the ideXlab platform.
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Marine-sulfated polysaccharides extract of Ulva armoricana green algae exhibits an antimicrobial activity and stimulates cytokine expression by intestinal epithelial cells
Journal of Applied Phycology, 2016Co-Authors: Mustapha Berri, Cindy Slugocki, Michel Olivier, Emmanuelle Helloin, Isabelle Jacques, Henri Salmon, Hervé Demais, Matthieu Goff, Pi Nyvall CollenAbstract:An aqueous marine-sulfated polysaccharide (MSP) extract, prepared from the green macroalga Ulva armoricana , was tested as an antibacterial compound against 42 bacterial strains and isolates found in livestock animals. Both Gram-positive and Gram-negative bacteria growths were affected. The most susceptible pathogens were Pasteurella multocida , Mannheimia haemolytica , Erysipelothrix rhusiopathiae , Staphylococcus aureus , and Streptococcus suis , with a minimum inhibitory concentration (MIC) ranging from 0.16 to 6.25 mg mL^−1. Enterococcus cecorum , Streptococcus dysgalactiae , Corynebacterium , Trueperella pyogenes , and Bordetella bronchiseptica strains were also susceptive to MSP with a complete inhibition recorded at MIC values of 25 and 50 mg mL^−1. The stimulation of the immune response mediators of the host’s gut with the extract was evaluated using an in vitro system of differentiated porcine intestinal epithelial cells (IPEC-1). RT-qPCR analysis showed a significant increase of mRNA expression of cytokines such as IL1α, IL1β, L6, IL8, TNFα, and TGFβ as well as the Chemokine CCL20. The extract also significantly induced the expression of PPARγ, a ligand-activated transcription factor, and TLR2 receptor.