Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disorder which is characterized by intense itch and inflammatory eczematous lesions. Keratinocytes are pivotal cells in the pathogenesis of AD as much as Th2 cells. Regulation of pro-inflammatory features of keratinocytes in combination with T cell modulators such as JAK inhibitors might hold promise for achieving disease control in AD patients better than T cell modulators alone. In this regards, targeting NLRP3 inflammasome (N3I) of keratinocytes and skin-infiltrating/resident myeloid cells might open new insight for AD patient’s therapy.
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