An intestinal epithelial defect conferring ER stress results in inflammation involving both innate and adaptive immunity.

In cultures from 20- to 24-week-old Winnie mice, there was a highly significant increase ( P <0.01) in the production of T H 1 (IL-12p70 and tumor necrosis factor-α), T H 2 (IL-3, IL-5, and IL-9), and T H 17 (IL-17A and IL-12/23p40) cytokines, and the chemokine monocyte chemotactic protein-1, and a less significant increase ( P <0.05) in other T H 1 (IL-1β and IFN-γ) and T H 2 (IL-10 and IL-13) cytokines, and the chemokines, keratinocyte chemoattractant and granulocyte colony-stimulating factor.

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