Abstract
but not in CD8αα+ IEL or LPL. Chromatin immunoprecipitation (CHIP) analysis from splenic CD8αβ T cells from TNF△ARE/+ but not wild type mice revealed selective recruitment of ATF6 and XBP1 to the Grp78 promoter. Consistent with the cytotoxic effect of TNF△ARE/ + derived CD8αβ+ T cells on the small intestinal epithelial cell line Mode-K, CHIP analysis revealed selective binding of ATF4, ATF6 and XBP1 to the granzyme B promoter in CD8αβ+ IEL from TNF△ARE/+ but not wild type mice. Finally, Grp78 knock down through the use of siRNA or the bacterial toxin EGF-SubA fusion protein completely abolished IFNγ and granzyme B expression. In conclusion, these results provide first evidence that ER stress response-associated mechanisms contribute to the cytotoxic effector function of CD8αβ+ IEL under condition of chronic ileitis in TNF△ARE/+ mice.
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