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- Title
Aryl hydrocarbon receptor engagement during redox alteration determines the fate of CD4<sup> </sup> T cells in C57BL/6 mice.
- Authors
Mohammadi, Hamidreza; Daryabor, Gholamreza; Ghaffarian Bahraman, Ali; Keshavarzi, Majid; Kalantar, Kurosh; Mohammadi‐Bardbori, Afshin
- Abstract
The preservation of the redox homeostasis is critical for cell survival and functionality. Redox imbalance is an essential inducer of several pathological states. CD4 /helper T cells are highly dependent on the redox state of their surrounding milieu. The potential of the aryl hydrocarbon receptor (AhR) engagement in controlling CD4 T‐cell fate during redox alteration is still challenging. C57BL/6 mice were treated with AhR agonist 6‐formylindolo[3,2‐b]carbazole (FICZ), AhR antagonist CH223191, an inhibitor of glutathione biosynthesis buthionine sulfoximine (BSO), and the antioxidant N‐acetylcysteine (NAC) alone or in combination. Six days later, splenocytes were evaluated for the expression of the redox‐related genes and the possible changes in T‐cell subsets. FICZ like BSO significantly elevated the expression of HMOX1, GCLC, and GCLM genes but it failed to increase the expression of the Nrf2 gene. Moreover, FICZ BSO increased while FICZ CH223191 or NAC decreased the expression of these genes. FICZ also significantly increased Th1 cell numbers but decreased Tregs in a dose‐dependent manner. Furthermore, a high dose of FICZ CH223191 NAC significantly enhanced Th1, Th17, and Treg cells but its low dose in such a situation increased Th2 and Th17 while decreased Treg cells. AhR engagement during redox alteration can determine the fate of CD4 T cells, so, AhR agonists or antagonists might be useful in assessing immune responses. However, these results need further verifications in vitro and in animal models of various diseases.
- Subjects
ARYL hydrocarbon receptors; LABORATORY mice; T cells; REGULATORY T cells; OXIDATION-reduction reaction; T cell receptors
- Publication
Journal of Biochemical & Molecular Toxicology, 2021, Vol 35, Issue 8, p1
- ISSN
1095-6670
- Publication type
Academic Journal
- DOI
10.1002/jbt.22821