Psoriasis: Treatment and Pathogenesis

This study uses a CRISPR screen and AI to identify new drug targets for psoriasis, finding ALOX5 and OXTR as promising candidates with validated therapeutic effects.

This study shows REV-ERBβ negatively regulates TH17-mediated inflammation in mouse models, acting independently from REV-ERB through distinct mechanisms.

The paper identifies HLA-C*06:02-presented peptides in psoriasis lesions, finding lesion-specific peptides linked to disease pathogenesis.

The paper compares IL-17-producing CD8+ T cells (Tc17) to CD4+ Th17 cells, showing differences in phenotype, metabolism, and cytokine production.

This study shows IFN-γ suppresses IL-17A-driven neutrophilic inflammation in the lungs via STAT1, revealing a regulatory interaction between TH1 and TH17 cells.

This study identifies Vγ4+ γδT17 cells as a link between psoriasis and MASLD, showing their role in systemic inflammation and hepatic remodeling, with clinical relevance of IL-17-targeted therapy.

This study identifies genetic risk factors associated with severe psoriasis and shows that polygenic risk scores can predict severe disease outcomes better than traditional risk factors.

This study identifies Gelsolin as a regulator of ER stress in psoriasis-like dermatitis, showing it counteracts inflammatory circuits driven by IMQ-induced organelle stress.

This study uses single-cell RNA sequencing to identify CD4+ T cell phenotypes in psoriasis patients associated with response to IL-23 blockade.

This study examines how psoriasis-like inflammation affects mitochondrial structure and function in keratinocytes and fibroblasts, revealing cell-specific changes.

This paper shows that inhibiting KDM6B reduces monocyte activation and skin inflammation in a psoriasis model by restoring H3K27me3 and suppressing inflammatory gene expression.

This study identifies prolactin as a mediator linking psychological stress to psoriasis through a fibroblast-chemokine pathway, showing that targeting PRL signaling reduces disease severity in mice.

The paper investigates the impact of a methyl group substitution in IL-17 inhibitors, finding that replacing a difluoro group with a methyl significantly improves safety and efficacy.

This study shows that A20's M1 ubiquitin binding motif suppresses TH17/22 cell activation and IL-22-driven enteritis by regulating RORγt and epigenetic changes in T cells.

This study shows that saturated fats drive psoriasis via FABP5-mediated IL-1β/IL-17 signaling in skin macrophages, exacerbating obesity-associated psoriasis.

The paper identifies CCR7+ dendritic cells as the primary source of IL-23 in psoriasis, linking them to type 17 inflammation and relapse.

The paper identifies a unique myeloid precursor population that facilitates the spread of psoriatic inflammation from skin to joints, interacting with fibroblasts to regulate T cell IL-17 expression.

This study shows that human dermal fibroblast spheroids reduce psoriasis severity in mice, with effects comparable to anti-IL-23 therapy and unique monocyte inhibition.

This study shows RUNX2 suppresses Th17 pathogenicity in MS and EAE by inhibiting neutrophil extracellular trap-driven Th17 priming.

The paper identifies TWEAK-IL-13 signaling as a driver of paradoxical skin reactions following anti-TNF, IL-17, or IL-23 therapy.

This study shows that a short-term high-fat diet during the onset of psoriasis worsens disease severity through immune system changes, even after returning to a normal diet.

This study identifies ALOX12B as a driver of skin inflammation through the inflammasome/Th17 signaling axis, showing its overexpression in psoriasis and atopic dermatitis and demonstrating a novel inhibitor's efficacy in a mouse model.

This study identifies PGAM as a negative regulator of Th17 pathogenicity using single-cell RNA-seq and metabolic flux analysis.

This study identifies Serpine1 as critical for Th17 cell differentiation and psoriasis, showing its therapeutic potential through genetic and pharmaceutical inhibition.

This study identifies sex-specific transcriptomic differences in psoriatic lesions through a meta-analysis, revealing distinct pathways and cell type abundances between males and females.

The paper shows how different T cell types drive distinct transcriptional changes in skin cells during inflammation, linking these changes to diseases like psoriasis and scleroderma.

This study performs a transcriptomic meta-analysis of 44 psoriasis studies to identify immune-related gene expression patterns and novel pathways involved in psoriasis pathogenesis.