The aryl hydrocarbon receptor in T cells contributes to sustaining oral tolerance against ovalbumin in a mouse model
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Date
2017-03-20
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Abstract
Oral tolerance (OT) towards antigens encountered in the gut is a vital immune function of gut
immunity. Experimental models can demonstrate OT efficacy by feeding of a protein followed by
peripheral immunization and measuring the specific antibody titer. We had previously shown that
exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a xenobiotic high-affinity aryl
hydrocarbon receptor (AhR)-ligand, destabilized OT against ovalbumin (OVA) in mice. AhR is
involved in the development, differentiation and function of immune cells, and highly expressed in
gut epithelial cells and gut immune cells. We here used AhR-deficient mice to study the role of AhR
in OT further. We show that complete AhR-deficiency undermines the stability of oral tolerance
against OVA upon multiple immunizations, despite no renewed oral encounter with the antigen. This
OT destabilization is accompanied by significant changes in IL10 and TGFß RNA in the gut tissue.
Using conditional AhR-deficient mouse lines, we identify T cells as the major responsible immune
cell type in this context. Our findings add to knowledge that lack of AhR signaling in the gut impairs important gut immune functions.
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Keywords
OT, Aryl hydrocarbon receptor, T cells, Mouse, Mucosal immunology