ArticleInflammation2025
Exploring the Common Pathogenic Mechanisms of Psoriasis and Atopic Dermatitis: The Interaction between SGK1 and TIGIT Signaling Pathways.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- High-Salt Diet Exacerbates Murine Imiquimod-Induced Psoriasis-like Dermatitis via Activation of Serum- and Glucocorticoid-Inducible Kinase 1.International journal of molecular sciences · 2026Article
- NK Cell Disfunction in Atopic Dermatitis: A Missing Link Between Type 2 Inflammation, Microbial Dysbiosis and Antiviral Immunity.International journal of molecular sciences · 2026Review
- Palmitic acid aggravates atopic dermatitis by regulating SGK1/NEDD4L-involved cutaneous neuroimmune inflammation through driving TRPV1 and MRGPRB2 S-palmitoylation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- The Effect of Glucocorticoid and Mineralocorticoid Receptor Antagonists in the Skin of Aged Female Mice.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aims to explore the common pathogenic mechanisms of psoriasis and atopic dermatitis, two T-cell-mediated autoimmune diseases. Utilizing single-cell transcriptomic sequencing data, we revealed that Treg cells primarily express TIGIT in both psoriasis and atopic dermatitis, and identified a subset of macrophages that highly express SGK1. These cells can interact with T cells via the NECTIN2-TIGIT signaling pathway, inhibiting the differentiation of T cells into a pro-inflammatory phenotype, thereby uncovering a common immunoregulatory mechanism in both diseases. Furthermore, we discovered that inhibition of SGK1 exacerbates the inflammatory response in disease models of both conditions. These findings not only provide a new perspective for a common therapeutic strategy for psoriasis and atopic dermatitis but also highlight the importance of considering these molecular interactions in future treatments. Validation of these observations through further qPCR, immunofluorescence, and animal studies has identified potential new targets for the treatment of psoriasis and atopic dermatitis.
Indexed as
Identifiers
39088121What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.