176 Myeloid cell-specific deletion of mTOR suppresses psoriasis-like skin inflammation in C57BL/6 mice

The pathophysiology of psoriasis, an autoimmune skin disorder, that affects approximately 3% the population worldwide, is incompletely understood, despite advanced knowledge. In this study, we investigated role and contribution mTOR signaling in myeloid lineage cells regulating pathogenesis systemic inflammation associated with psoriasis. We first established a genetic mouse model which was specifically deleted using Cre-lox technology to test myeloid-specific psoriasis imiquimod (IMQ)-induced significance depletion bridging adaptive immune response deficient mice (mTORflox/flox/ LysMcre+/+; mTORmyeKO) flox-only control LysMcre-/-; floxed) were treated IMQ end-points measured at day 6 after necropsy. Interestingly, mTORmyeKO exhibited less pronounced psoriasiform lesions, decreased PASI scores, epidermal thickness, suppressed hyperplasia, parakeratosis, rete ridges, Munro microabscesses dermal infiltratory compared mTORfloxed showed disease characteristics (p<0.01). Furthermore, observed significant decrease levels activated helper T-lymphocytes (cd4/cd8+), dendritic cells(cd11), macrophages (F4/80) lesions when (p<0.001). summary, our data show ablation confers resistance imiquimod-induced psoriasis-like dermatitis mice. This suggests or pharmacological targeting cells' axes may help alleviate disease.