The
integrin αE known as CD103 binds
integrin β7 to form the complete heterodimeric
integrin molecule αEβ7. CD103 is mainly expressed by lymphocytes within epithelial tissues of intestine, lung, and skin as well as subsets of mucosal and dermal conventional dendritic cells (
cDCs). CD103 has been originally implicated in the attachment of lymphocytes to epithelium in the gut and skin through the interaction with
E-cadherin expressed on intestinal epithelial cells, keratinocytes, and Langerhans cells (LCs). However, an impact of CD103 on the cutaneous immune responses and the development of inflammatory
skin diseases remains elusive. Here, we report that CD103 regulates the development of psoriasiform
dermatitis through the control of the function of
cDCs. Deficiency in CD103 exacerbates psoriasiform
dermatitis, accompanied by excessive epidermal
hyperplasia and infiltration of inflammatory leukocytes. Furthermore, deficiency in CD103 not only accelerates the production of proinflammatory
cytokines in psoriatic lesions but also promotes the generation of lymphocytes producing
interleukin (IL)-17 in the skin-draining peripheral lymph nodes (PLNs). Under the deficiency in CD103,
cDCs localized in PLNs enhance
cytokine production following activation. Thus, our findings reveal a pivotal role for CD103 in the control of the function of
cDCs to regulate cutaneous
inflammation in psoriasiform
dermatitis.