scholarly journals T-bet over-expression regulates aryl hydrocarbon receptor-mediated T helper type 17 differentiation through an interferon (IFN)γ-independent pathway

2017 ◽  
Vol 188 (1) ◽  
pp. 22-35 ◽  
Author(s):  
M. Yokosawa ◽  
Y. Kondo ◽  
M. Tahara ◽  
M. Iizuka-Koga ◽  
S. Segawa ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
T Helper ◽  
Over Expression ◽  
Aryl Hydrocarbon ◽  
Ifn Γ ◽  
Helper Type

Mo1727 Impaired Expression of the Aryl Hydrocarbon Receptor and CD39 Is Associated With Heightened Pathogenicity of T Helper Type 17 Cells in Crohn's Disease

2014 ◽  
Vol 146 (5) ◽  
pp. S-645
Author(s):  
Maria Serena Longhi ◽  
Alireza Kalbasi ◽  
Byron P. Vaughn ◽  
Barbara Wegiel ◽  
Alan C. Moss ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Aryl Hydrocarbon Receptor ◽  
T Helper ◽  
Aryl Hydrocarbon ◽  
Helper Type

scholarly journals Activation of the aryl hydrocarbon receptor during development enhances the pulmonary CD4+ T-cell response to viral infection

2015 ◽  
Vol 309 (3) ◽  
pp. L305-L313 ◽  
Author(s):  
Lisbeth A. Boule ◽  
Bethany Winans ◽  
Kris Lambert ◽  
Beth A. Vorderstrasse ◽  
David J. Topham ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Aryl Hydrocarbon Receptor ◽  
Respiratory Infection ◽  
T Cell Responses ◽  
T Cell Subsets ◽  
T Helper ◽  
Cell Responses ◽  
Aryl Hydrocarbon ◽  
Helper Type

Respiratory infections are a threat to health and economies worldwide, yet the basis for striking variation in the severity of infection is not completely understood. Environmental exposures during development are associated with increased severity and incidence of respiratory infection later in life. Many of these exposures include ligands of the aryl hydrocarbon receptor (AHR), a transcription factor expressed by immune and nonimmune cells. In adult animals, AHR activation alters CD4+ T cells and changes immunopathology. Developmental AHR activation impacts CD4+ T-cell responses in lymphoid tissues, but whether skewed responses are also present in the infected lung is unknown. To determine whether pulmonary CD4+ T-cell responses are modified by developmental AHR activation, mice were exposed to the prototypical AHR ligand 2,3,7,8-tetrachlorodibenzo- p-dioxin during development and infected with influenza virus as adults. Lungs of exposed offspring had greater bronchopulmonary inflammation compared with controls, and activated, virus-specific CD4+ T cells contributed to the infiltrating leukocytes. These effects were CD4+ T cell subset specific, with increases in T helper type 1 and regulatory T cells, but no change in the frequency of T helper type 17 cells in the infected lung. This is in direct contrast to prior reports of suppressed conventional CD4+ T-cell responses in the lymph node. Using adoptive transfers and manipulating the pathogen properties, we determined that developmental exposure influenced factors intrinsic and extrinsic to CD4+ T cells and may involve developmentally induced changes in signals from infected lung epithelial cells. Thus developmental exposures lead to context-dependent changes in pulmonary CD4+ T-cell subsets, which may contribute to differential responses to respiratory infection.

scholarly journals Galactomyces fermentation filtrate prevents T helper 2‐mediated reduction of filaggrin in an aryl hydrocarbon receptor‐dependent manner

2015 ◽  
Vol 40 (7) ◽  
pp. 786-793 ◽  
Author(s):  
K. Takei ◽  
C. Mitoma ◽  
A. Hashimoto‐Hachiya ◽  
M. Takahara ◽  
G. Tsuji ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Dependent Manner ◽  
T Helper ◽  
T Helper 2 ◽  
Aryl Hydrocarbon ◽  
Mediated Reduction

scholarly journals IFN-γ–Producing T-Helper 17.1 Cells Are Increased in Sarcoidosis and Are More Prevalent than T-Helper Type 1 Cells

2016 ◽  
Vol 193 (11) ◽  
pp. 1281-1291 ◽  
Author(s):  
Joris Ramstein ◽  
Caroline E. Broos ◽  
Laura J. Simpson ◽  
K. Mark Ansel ◽  
Sara A. Sun ◽  
...  
Keyword(s):  
T Helper ◽  
Ifn Γ ◽  
Helper Type

Cyclophosphamide modulates CD4+ T cells into a T helper type 2 phenotype and reverses increased IFN-γ production of CD8+ T cells in secondary progressive multiple sclerosis

2004 ◽  
Vol 146 (1-2) ◽  
pp. 189-198 ◽  
Author(s):  
Arnon Karni ◽  
Konstantin Balashov ◽  
Wayne W. Hancock ◽  
Padmanabhan Bharanidharan ◽  
Michal Abraham ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
T Cells ◽  
Cd8 T Cells ◽  
Cd4 T Cells ◽  
Progressive Multiple Sclerosis ◽  
T Helper ◽  
Secondary Progressive ◽  
Ifn Γ ◽  
Helper Type

scholarly journals Role of the Aryl Hydrocarbon Receptor in the Immune Response Profile and Development of Pathology during Plasmodium berghei Anka Infection

2014 ◽  
Vol 82 (8) ◽  
pp. 3127-3140 ◽  
Author(s):  
Fatima Brant ◽  
Aline S. Miranda ◽  
Lisia Esper ◽  
David Henrique Rodrigues ◽  
Lucas Miranda Kangussu ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Plasmodium Berghei ◽  
Transforming Growth Factor ◽  
Interleukin 17 ◽  
High Morbidity ◽  
Content Type ◽  
Aryl Hydrocarbon ◽  
Tnf Α ◽  
Ifn Γ ◽  
The Brain

ABSTRACTInfection withPlasmodium falciparummay result in severe disease affecting various organs, including liver, spleen, and brain, resulting in high morbidity and mortality.Plasmodium bergheiAnka infection of mice recapitulates many features of severe human malaria. The aryl hydrocarbon receptor (AhR) is an intracellular receptor activated by ligands important in the modulation of the inflammatory response. We found that AhR-knockout (KO) mice infected withP. bergheiAnka displayed increased parasitemia, earlier mortality, enhanced leukocyte-endothelial cell interactions in the brain microvasculature, and increased inflammation in brain (interleukin-17 [IL-17] and IL-6) and liver (gamma interferon [IFN-γ] and tumor necrosis factor alpha [TNF-α]) compared to infected wild-type (WT) mice. Infected AhR-KO mice also displayed a reduction in cytokines required for host resistance, including TNF-α, IL-1β, and IFN-γ, in the brain and spleen. Infection of AhR-KO mice resulted in an increase in T regulatory cells and transforming growth factor β, IL-6, and IL-17 in the brain. AhR modulated the basal expression of SOCS3 in spleen and brain, andP. bergheiAnka infection resulted in enhanced expression of SOCS3 in brain, which was absent in infected AhR-KO mice. These data suggest that AhR-mediated control of SOCS3 expression is probably involved in the phenotype seen in infected AhR-KO mice. This is, to our knowledge, the first demonstration of a role for AhR in the pathogenesis of malaria.

scholarly journals Human Mesenchymal Stem Cells Modulate Cellular Immune Response to Islet Antigen Glutamic Acid Decarboxylase in Type 1 Diabetes

2010 ◽  
Vol 95 (8) ◽  
pp. 3788-3797 ◽  
Author(s):  
Maria M. Zanone ◽  
Enrica Favaro ◽  
Ilaria Miceli ◽  
Giorgio Grassi ◽  
Elisa Camussi ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Acid Decarboxylase ◽  
Diabetic Patients ◽  
Human Mscs ◽  
T Helper ◽  
Ifn Γ ◽  
Islet Antigen ◽  
Helper Type

Context: Mesenchymal stem cells (MSCs) exert an immunosuppressive effect on the immune system. However, studies on the immunomodulatory potential of MSCs in type 1 diabetes are lacking. Objective: We aimed to evaluate whether human MSCs may inhibit in vitro pancreatic islet antigen-specific T cell activation in type 1 diabetes. Design: Human MSCs were isolated and characterized. Peripheral blood mononuclear cells (PBMCs) were obtained from nine type 1 diabetic patients at disease onset and 13 healthy control subjects. IFN-γ, IL-10, and IL-4 enzyme-linked immunospot responses of lymphocytes incubated with glutamic acid decarboxylase 65 (GAD65) were investigated in PBMC cultures and PBMC/MSC cocultures. Levels of prostaglandin E2 (PGE2), IFN-γ, IL-4, and IL-10 in supernatants were measured by ELISA. PGE2 inhibition experiments with NS-398 and indomethacin were also performed. Results: Five diabetic patients were identified with a positive PBMC IFN-γ response to GAD65 and negative IL-10 and IL-4 response. PBMC/MSC cocultures resulted in a significant decrease in the number of spots and in detection of IL-4-secreting cells. PGE2 inhibitors abrogated the immune-suppressive effect, indicating an involvement of PGE2 production, and the constitutive production of PGE2 by MSCs was enhanced in PBMC/MSC coculture. Moreover, in GAD-responder patients, GAD-stimulated PBMC/MSC cocultures significantly decreased secretion of IFN-γ and IL-10 and increased secretion of IL-4. Conclusions: These results provide evidence that human MSCs abrogate in vitro a proinflammatory T helper type 1 response to an islet antigenic stimulus in type 1 diabetes. MSCs induce IL-4-producing cells, suggesting a possible switch to an antiinflammatory T helper type 2 signaling of T cells.

scholarly journals The Aryl Hydrocarbon Receptor: Differential Contribution to T Helper 17 and T Cytotoxic 17 Cell Development

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e106955 ◽  
Author(s):  
Mark D. Hayes ◽  
Vitalijs Ovcinnikovs ◽  
Andrew G. Smith ◽  
Ian Kimber ◽  
Rebecca J. Dearman
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Cell Development ◽  
T Helper ◽  
T Helper 17 ◽  
Aryl Hydrocarbon ◽  
Differential Contribution
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