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Learn MoreUsing lineage-tracing in a well-established psoriasis-like mouse model with inducible epidermal deletion of c-Jun and JunB, we found that mutant HF-SCs survive and express a broad group of pro-inflammatory cytokines, whereas mutant inter-follicular epidermal cells (IFE) disappear over time. Mutant HF-SCs initiate epidermal hyperplasia and skin inflammation by priming neighboring non-mutant epidermal cells to acquire a psoriasis-like phenotype. To explore the molecular mechanisms that govern the behavior of these distinct mutant and non-mutant HF-SCs and IFE cell populations during psoriasis-like disease, RNA sequencing analyses of sorted GFP+, Tomato+ HF-SCs and b-KCs from DKO*-mT/mG mice. SOURCE: Osvaldo GrañaBioinformatics Unit CNIO
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