Upregulation of aryl hydrocarbon receptor expression in CD4 T lymphocytes during an immune response in vivo. (INM1P.431)

Abstract

Abstract Activation of the aryl hydrocarbon receptor (AHR) can impact T-cell differentiation and the maintenance of tissue-resident T cells. AHR expression, measured by RT-PCR or Western blot has been shown to be low in most CD4 T-cell subsets with highest expression found after stimulation of naïve CD4 T cells under Th17 conditions in vitro. The current study measures AHR expression within CD4 T-cell subsets of naïve or skin-grafted mice using flow cytometry. Cells were freshly isolated from the spleen, lymph nodes or skin of either untreated mice or mice that underwent allogeneic skin transplant. AHR expression in cells from untreated mice was highest in IL-17A+ CD4 T cells, followed by FoxP3+ and IFNγ+ cells. Naïve, CD62L+ CD4 T cells had the lowest expression. AHR expression in splenic or lymph node CD4 T cells from skin-grafted mice was similar to naïve mice with 20 - 30 % of FoxP3+ and <10% of FoxP3- being AHR+. However, CD4 T cells within the skin grafts showed elevated AHR expression compared to spleen or LN with 75 - 85 % of FoxP3+ and 40 - 70% of FoxP3- being AHR+. This is comparable to the >90% AHR+ CD4 T cells found when splenocytes were stimulated in vitro with anti-CD3 antibody in the presence of TGFb and IL-6. We conclude that the up-regulation of AHR expression in CD4 T cells in vitro also happens during immune responses in vivo and is not restricted to a single T cell subset, and may be important in T cell differentiation, trafficking, and cytokine production.