The skin has three main layers—epidermis, dermis, and hypodermis—that work together as a physical and immune barrier. This review explains how disruptions in that barrier network contribute to psoriasis and how those insights relate to current and emerging treatments. The epidermis forms the main “seal,” with the stratum corneum and tight junctions limiting water loss and blocking pathogens and irritants. The dermis provides structural support and contains many immune cells, while keratinocytes also help defend the skin by releasing antimicrobial molecules and inflammatory signals when triggered.

Psoriasis is described as a chronic inflammatory skin disease driven largely by immune dysregulation that promotes keratinocyte hyperproliferation and abnormal differentiation, leading to barrier dysfunction and characteristic lesions. Physical barrier changes include altered keratin/differentiation markers, disrupted cell-cell junction proteins, and lipid-matrix shifts in the stratum corneum that contribute to water loss and inflammation. Cytokines such as IL-17 and IL-22 play key roles. Immune dysfunction spans innate and adaptive activation (notably Th17/Tc17 pathways) alongside impaired regulatory responses, helping explain persistence and recurrence. The review also covers genetic and environmental contributors and summarizes treatment options—from topicals and phototherapy to systemic agents and biologics targeting TNF-α, IL-17, and IL-23—plus directions for future therapy and patient stratification.

Reference: Orsmond A, Bereza-Malcolm L, Lynch T, March L, Xue M. Skin Barrier Dysregulation in Psoriasis. Int J Mol Sci. 2021 Oct 7;22(19):10841. doi: 10.3390/ijms221910841. PMID: 34639182; PMCID: PMC8509518.

Psoriasis and lichen planus often look similar and can be difficult to distinguish consistently in routine practice, especially given the volume of skin conditions and limited access to experienced dermatologists. To address this, researchers trained a deep-learning image classifier based on a customized ResNet-50 convolutional neural network to differentiate only these two conditions. They used DermNet images, applied class balancing and data augmentation to address dataset imbalance and improve variety, and validated performance using multiple approaches (random train/test split plus 3- and 5-fold cross-validation). The model achieved performance around the high 80% range for accuracy and similar values for sensitivity and specificity, suggesting computer-aided image classification could support timely identification of look-alike dermatoses.

The paper also situates its work within a broader body of research applying deep learning to dermatology, noting that many prior studies focus on psoriasis alone, group psoriasis and lichen planus together, or use datasets that may not generalize well across settings. The authors emphasize isolating these two highly similar diseases is important for clinically useful differentiation, and describe preprocessing steps (cropping, watermark removal, resizing) to standardize images. Ultimately, they recommend larger datasets and further optimization to strengthen reliability and generalizability.

Reference: Eskandari A, Sharbatdar M. Efficient diagnosis of psoriasis and lichen planus cutaneous diseases using deep learning approach. Sci Rep. 2024 Apr 27;14(1):9715. doi: 10.1038/s41598-024-60526-4. PMID: 38678100; PMCID: PMC11055920.

Short-term, high-dose induction with risankizumab (an IL-23 inhibitor) produced durable plaque psoriasis control in a small proof-of-principle study, alongside a marked reduction in skin resident memory T cells (TRM). Among 20 adults randomized to 300 mg or 600 mg (given at baseline, Week 4, and Week 12/16 per the report), most achieved strong clinical responses through 52 weeks: 83% reached Psoriasis Area and Severity Index (PASI) 75, >60% reached PASI 90, and 43% reached PASI 100. Biopsies and single-cell analyses showed that lesional skin at baseline contained many T-cell populations, but by Week 52 the treated lesional skin looked more like nonlesional skin, with TRM—including IL-17–producing TRM17—significantly reduced (reported P=0.04). The higher dose appeared to more completely deplete T cells in tissue, though overall clinical efficacy looked similar between dose groups.

The investigators framed the findings as supportive of a “hit hard, hit early” hypothesis: if TRM help drive recurrence at the same sites, reducing/eradicating these cells via IL-23 blockade might extend remission after treatment withdrawal—potentially more so in patients with shorter disease duration. However, the presenter cautioned this is not a cure. Some patients remained clear well into year 2, while others gradually relapsed. The authors emphasized that larger prospective studies are needed to confirm whether high-induction regimens can reliably induce longer remissions and to better define durability, optimal dosing, and patient characteristics linked to sustained clearance.

Reference: Bankhead C. Short-Term High-Dose Psoriasis Therapy Shows Potential for Long-Term Disease Control. MedPage Today. Published March 13, 2024. Accessed January 27, 2026. https://www.medpagetoday.com/meetingcoverage/aad/109148?xid=nl_mpt_morningbreak2024-03-14&eun=g1443091d0r&utm_source=Sailthru&utm_medium=email&utm_campaign=MorningBreak_031424&utm_term=NL_Gen_Int_Daily_News_Update_active