Abstract
Many inflammatory diseases of the skin including atopic dermatitis (AD) and psoriasis are characterized by altered epidermal differentiation, but the mechanisms for such changes have remained unclear, in particular given their diverse immunologic pathogenesis. Here we show that IRAK2, a member of the signaling complex downstream of IL-1/IL-36, correlates positively with disease severity in both AD and psoriasis. IRAK2 brings together pro-inflammatory and differentiation dependent responses and this function of IRAK2 is specific to keratinocytes.
Full Text 
Sign-in/Register to access full text options
Sign-in/Register to access full text options 
Published version (
Free)
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
