Finally, in a mice model mimicking human acute AD lesions, the expression of KC-derived IL-33 was augmented and this cytokine was related to an anti-inflammatory effect on the disease [178]; however, in an AD-model in mice overexpressing IL-33, the levels of epidermal claudin 1 were reduced and IL-33 was also able to down-regulate the expression of this TJ protein in KCs assayed in vitro [179], which suggests a possible dual role of IL-33 in AD pathogenesis. This evidence concerns the gene CALCA and Alzheimer disease.