Psoriasis, a complex and recurrent chronic inflammatory skin disease involving various inflammatory cell types, requires effective cell communication to maintain the homeostatic balance of inflammation. However, patterns of communication at the single-cell level have not been systematically investigated. In this study, we employed social network analysis tools, pattern recognition, and manifold learning to compare molecular communication features between psoriasis cells and normal skin cells. Utilizing a process that facilitates the discovery of cell type-specific regulons, we analyzed internal regulatory networks among different cells in psoriasis. Advanced techniques for the quantitative detection of non-targeted proteins in pathological tissue sections were employed to demonstrate protein expression. Our findings revealed a synergistic interplay among the communication signals of immune cells in psoriasis. B-cells were activated, while Langerhans cells shifted into the primary signaling output mode to fulfill antigen presentation, mediating T-cell immunity. In contrast to normal skin cells, psoriasis cells shut down numerous signaling pathways, influencing the balance of skin cell renewal and differentiation. Additionally, we identified a significant number of active cell type-specific regulons of resident immune cells around the hair follicle. This study unveiled the molecular communication features of the hair follicle cell-psoriasis axis, showcasing its potential for therapeutic targeting at the single-cell level. By elucidating the pattern of immune cell communication in psoriasis and identifying new molecular features of the hair follicle cell-psoriasis axis, our findings present innovative strategies for drug targeting to enhance psoriasis treatment.

Background. Basan syndrome is a rare autosomal-dominant ectodermal dysplasia with certain clinic-pathological features caused by mutations in the SMARCAD1 gene. Currently, no skin malignancy related to Basan syndrome has been reported. This study was aimed at identifying related gene mutations in a new Chinese pedigree with Basan syndrome and discovering the possible association between Basan syndrome and cutaneous squamous cell carcinoma (cSCC). Methods. We report a case of Basan syndrome from China with family history of cSCC. The pedigree contains 28 individuals. Among them, 12 members had Basan syndrome, while 4 affected members were diagnosed with cSCC in the 1st and 2nd generations. Whole exome sequencing (WES) and Sanger sequencing were performed for 7 available individuals. The specific gene mutation on pre-mRNA splicing was also analyzed using in vitro Minigene assay. In addition, sequencing data was analyzed with bioinformatics workflow, aiming to discover the gene associated with cSCC. Results. Gene sequencing results showed a heterozygous mutation, c.378+5GA, in the SMARCAD1 gene in all tested individuals with Basan syndrome. Minigene result implicated the specific mutation may cause splicing variations by exon skipping occurring in the targeted exons. Conclusion. To the best of our knowledge, this is the first study reported Basan syndrome with family history of cSCC. Despite in this study we cannot draw any conclusion about the association between Basan syndrome and cSCC at the genetic level, this study encourages future works to substantiate this potential but important issue.

Background: Androgen has been regarded as the strongest stimulator of sebum formation and sebocyte proliferation in individuals with acne. However, the underlying mechanisms remain to be elucidated. Recent studies suggest that autophagy is involved in lipid degradation and the regulation of cell proliferation. This study aims to explore the effects of testosterone on autophagy and its potential contribution to lipid accumulation and sebocyte proliferation. Methods: Human SZ95 sebocytes were cultured with linoleic acid (LA) to induce sebum production. This study examined the role of testosterone in acne development by measuring autophagy, lipid accumulation, and cell proliferation. To determine whether testosterone's effects on acne depend on autophagy, the autophagy inducer rapamycin and the inhibitor 3-methyladenine (3-MA) were used in combination with LA. Results: The results indicated that treatment with testosterone decreased the levels of LC-3II (p < 0.01) and Beclin 1 (p < 0.01) while increasing p62 level (p < 0.05) in SZ95 cells. Additionally, testosterone treatment induced lipid accumulation, as demonstrated by Oil Red O staining (p < 0.01), and increased Triglyceride (TG) content (p < 0.01) in SZ95 cells. Moreover, testosterone treatment increased cell viability in SZ95 cells according to the 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay (p < 0.01) and increased the count of Ki67 positive cells in immunofluorescent staining (p < 0.01). Co-treatment with rapamycin reversed the effects of testosterone on autophagy (p < 0.05 or p < 0.01), lipid accumulation (p < 0.01), and sebocyte proliferation (p < 0.01). In contrast, treatment with 3-MA mimicked all the aforementioned effects of testosterone (p < 0.05 or p < 0.01). Furthermore, immunoblot analysis revealed that treatment with testosterone enhanced the phosphorylation of v-akt murine thymoma viral oncogene homolog (AKT) (p < 0.01) and the mammalian target of rapamycin (mTOR) (p < 0.05), which were counteracted by rapamycin (p < 0.05 or p < 0.01) but mimicked by 3-MA (p < 0.05). Conclusions: These findings suggest that testosterone may facilitate acne progression by activating mTOR and subsequently inhibiting autophagy.