scholarly journals DNA Methylation Patterns in CD4+ T Cells of Naïve and Influenza A Virus-Infected Mice Developmentally Exposed to an Aryl Hydrocarbon Receptor Ligand

2021 ◽  
Vol 129 (1) ◽  
pp. 017007 ◽  
Author(s):  
Catherine G. Burke ◽  
Jason R. Myers ◽  
Christina M. Post ◽  
Lisbeth A. Boulé ◽  
B. Paige Lawrence
Keyword(s):  
Dna Methylation ◽  
T Cells ◽  
Aryl Hydrocarbon Receptor ◽  
Influenza A Virus ◽  
Cd4 T Cells ◽  
Influenza A ◽  
Receptor Ligand ◽  
Aryl Hydrocarbon Receptor Ligand ◽  
Aryl Hydrocarbon ◽  
Methylation Patterns

scholarly journals An aryl hydrocarbon receptor ligand acts on dendritic cells and T cells to suppress the Th17 response in allergic rhinitis patients

2014 ◽  
Vol 94 (5) ◽  
pp. 528-535 ◽  
Author(s):  
Ping Wei ◽  
Guo-hua Hu ◽  
Hou-yong Kang ◽  
Hong-bing Yao ◽  
Wei Kou ◽  
...  
Keyword(s):  
T Cells ◽  
Allergic Rhinitis ◽  
Dendritic Cells ◽  
Aryl Hydrocarbon Receptor ◽  
Receptor Ligand ◽  
Th17 Response ◽  
Aryl Hydrocarbon Receptor Ligand ◽  
Aryl Hydrocarbon

An endogenous aryl hydrocarbon receptor ligand enhances de novo generation of regulatory T cells in humans

2018 ◽  
Vol 105 (2) ◽  
pp. 291-295 ◽  
Author(s):  
Imen Zamali ◽  
Raja Rekik ◽  
Nadia Belhadj Hmida ◽  
Ahlem Ben Hmid ◽  
Ons Kammoun ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Aryl Hydrocarbon Receptor ◽  
De Novo ◽  
Receptor Ligand ◽  
Aryl Hydrocarbon Receptor Ligand ◽  
Aryl Hydrocarbon

scholarly journals Cytokine Regulation in Human CD4 T Cells by the Aryl Hydrocarbon Receptor and Gq-Coupled Receptors

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Jeremy P. McAleer ◽  
Jun Fan ◽  
Bryanna Roar ◽  
Donald A. Primerano ◽  
James Denvir
Keyword(s):  
T Cells ◽  
Aryl Hydrocarbon Receptor ◽  
Cd4 T Cells ◽  
Cytokine Regulation ◽  
Aryl Hydrocarbon

ARYL HYDROCARBON RECEPTOR LIGAND ACTIVITY OF POLYCYCLIC AROMATIC KETONES AND POLYCYCLIC AROMATIC QUINONES

2007 ◽  
Vol 26 (7) ◽  
pp. 1370 ◽  
Author(s):  
Kentaro Misaki ◽  
Hirofumi Kawami ◽  
Tota Tanaka ◽  
Hiroshi Handa ◽  
Masafumi Nakamura ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Receptor Ligand ◽  
Aromatic Ketones ◽  
Aryl Hydrocarbon Receptor Ligand ◽  
Aryl Hydrocarbon ◽  
Polycyclic Aromatic ◽  
Ligand Activity

Activation of the aryl hydrocarbon receptor increases pulmonary neutrophilia and diminishes host resistance to influenza A virus

2005 ◽  
Vol 289 (1) ◽  
pp. L111-L124 ◽  
Author(s):  
Sabine Teske ◽  
Andrea A. Bohn ◽  
Jean F. Regal ◽  
Joshua J. Neumiller ◽  
B. Paige Lawrence
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Influenza A Virus ◽  
Influenza A ◽  
Viral Infections ◽  
Inflammatory Responses ◽  
Neutrophil Function ◽  
Aryl Hydrocarbon ◽  
Potent Agonist

Unlike their role in bacterial infection, less is known about the role of neutrophils during pulmonary viral infection. Exposure to pollutant 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD, dioxin) results in excess neutrophils in the lungs of mice infected with influenza A virus. TCDD is the most potent agonist for the aryl hydrocarbon receptor (AhR), and exposure to AhR ligands has been correlated with exacerbated inflammatory lung diseases. However, knowledge of the effects of AhR agonists on neutrophils is limited. Likewise, the factors regulating neutrophil responses during respiratory viral infections are not well characterized. To address these knowledge gaps, we determined the in vivo levels of KC, MIP-1α, MIP-2, LIX, IL-6, and C5a in infected mouse lungs. Our data show that these neutrophil chemoattractants are generally produced transiently in the lung within 12–24 h of infection. We also report that expression of CD11a, CD11b, CD49d, CD31, and CD38 is increased on pulmonary neutrophils in response to influenza virus. Using AhR-deficient mice, we demonstrate that excess neutrophilia in the lung is mediated by activation of the AhR and that this enhanced neutrophilia correlates directly with decreased survival in TCDD-exposed mice. Although AhR activation results in more neutrophils in the lungs, we show that this is not mediated by deregulation in levels of common neutrophil chemoattractants, expression of adhesion molecules on pulmonary neutrophils, or delayed death of neutrophils. Likewise, exposure to TCDD did not enhance pulmonary neutrophil function. This study provides an important first step in elucidating the mechanisms by which AhR agonists exacerbate pulmonary inflammatory responses.

scholarly journals Features of immune response against influenza infection in animals vaccinated with recombinant cross-protective vaccine

2019 ◽  
Vol 9 (3-4) ◽  
pp. 485-494
Author(s):  
L. M. Tsybalova ◽  
L. A. Stepanova ◽  
A. V. Korotkov ◽  
M. A. Shuklina ◽  
M. V. Zaitseva ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Influenza Virus ◽  
Influenza A Virus ◽  
Cd4 T Cells ◽  
Influenza A ◽  
Influenza Infection ◽  
Sublethal Dose ◽  
Universal Vaccine ◽  
Toll Like Receptor 5

Generating cross-reactive vaccines aimed at targeting all human influenza A virus subtypes is among high priority tasks in contemporary vaccinology. Such vaccines will be primarily demanded during pre-pandemic period as well as used to prime some population cohorts prior to vaccination with standard vaccines containing area-relevant epidemic virus. Unlike routine approach universal vaccines do not induce a sterilizing immunity, but significantly ameliorate overt infection and probable complications. Our study was aimed at evaluating characteristics of immune response in experimental animals primed with a candidate universal vaccine challenged with sublethal influenza A virus infection. Mice were immunized intranasally with the recombinant protein FlgH2-2-4M2e containing conservative peptides derived from two influenza A virus proteins: M2 protein ectodomain and 76–130 amino acid sequence from the second hemagglutinin (HA2) subunit genetically linked to bacterial flagellin protein, which is a ligand for Toll-like receptor 5 (TLR5). Control mice received saline. Two weeks after immunization, mice from both groups were infected with a sublethal dose of A/Aichi/2/68 AN3N2 influenza virus strain. Level of immunoglobulins G and A in the blood sera and bronchoalveolar lavages (BAL) were determined two weeks after immunization and 1 month post infection. Percentage of lung CD4+ T and CD4+ Tem (CD44+CD62L–) cells secreting cytokines TNFα, IFNγ, IL-2 was determined. Immunized vs. control mice responded to sublethal infection with the influenza virus by insignificant weight loss and more pronounced production of vaccine peptide-specific (M2e and aa76–130 HA2) and pan-influenza A/Aichi/2/68 virus IgG and A in the blood sera and BAL. After challenge the number of CD4+ T cells secreting cytokines TNFα and/or IL-2 in immunized mice significantly exceeded counterpart T cells in unimmunized animals that was true for both CD4+T and CD4+ Tem cells. Memory CD4+ T cells were previously shown to play a key role in the prime-boost event and heterosubtypic immune response. Thus, we were able to demonstrate a priming effect for recombinant cross-protective vaccine used in our experiment.

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