Abstract

Imiquimod (IMQ), a TLR 7/8 agonist, was shown to induce a self-limited Th17-dominated contact dermatitis in healthy skin, but not the full picture of psoriasis. Whilst such an innate “first strike” of IMQ is needed for inducing inflammation, a “second strike” might perpetuate inflammation and induce the characteristic phenotype of psoriatic plaques. Here, IMQ was tested on clinically healed plaques of 5 psoriasis patients for inducing a “second strike”, namely the activation of CD103+ tissue-resident memory T cells (TRM) that recognize specific cutaneous antigens and thereby maintain the inflammatory response in the skin.

Full Text
Published version (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