De, Abhishek

ABSTRACT Tissue‐resident memory T cells (TRMs) are a distinct memory T‐cell subset that permanently reside in tissues such as the skin. In chronic immune‐mediated dermatoses, including psoriasis, atopic dermatitis, and vitiligo, TRMs are implicated in site‐specific “disease memory,” contributing to persistence and relapse at previously affected sites. This review synthesizes emerging concepts on TRMs in chronic inflammatory skin diseases and discusses clinical and translational implications, including TRM‐targeted therapies. Original human, animal, or in vitro studies evaluating TRMs in the pathogenesis or persistence of dermatologic diseases were included. In psoriasis, CD8 + TRMs (CD69 + CD103 + ) persisted in clinically healed skin. For atopic dermatitis, both CD4 + and CD8 + TRMs are implicated in maintaining Th2/Th22 inflammation. In vitiligo, autoreactive CD8 + TRMs at lesional margins mediate melanocyte destruction. Across dermatological diseases, TRMs share three core features: persistence in previously affected skin after clinical resolution, rapid reactivation by diverse triggers (stress, autoantigens, allergens, or cytokines) leading to site‐specific recurrence, and relative resistance to conventional therapies. Together, these properties provide a unifying framework linking tissue immune memory to the chronic, relapsing nature of inflammatory skin diseases. However, the dominant TRM pathways vary by disease, reflecting differences in immune polarization and antigen specificity. Targeting TRMs represents a promising strategy for disease control and serves as a biomarker of residual disease or flare. image

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by pruritus and eczematous lesions. Abrocitinib, a selective Janus kinase 1 (JAK1) inhibitor, has recently been approved in India for moderate-to-severe AD in adults. This prospective real-world case series evaluated the effectiveness and safety of abrocitinib in patients with moderate-to-severe AD who showed an inadequate response to cyclosporine. Nine patients (five females, four males; mean age 19.44 ± 7.68 years, range 10–34 years) were included. Three were adolescents or children in whom abrocitinib was used off-label. The mean disease duration was 13.33 ± 8.06 years, and eight patients had a positive family history of AD. Prior treatments included cyclosporine, methotrexate, and systemic corticosteroids. Abrocitinib was prescribed at a mean dose of 177.77 ± 44.09 mg daily (seven patients received 200 mg, two received 100 mg). Effectiveness was assessed at baseline and weeks 2, 4, 8, and 12 using the Eczema Area and Severity Index (EASI), Investigator’s Global Assessment (IGA), and Peak Pruritus Numerical Rating Scale (PP-NRS). Significant and progressive reductions were observed in all scores. Mean EASI decreased from 48.22 ± 7.88 at baseline to 6.33 ± 3.35 at week 12 ( P < 0.0001). IGA scores improved from 4 to 1.22 ± 0.44, while PP-NRS declined from 8.44 ± 0.52 to 2 ± 0.86 by week 12, with significance evident early in treatment. Most patients demonstrated good adherence, and dose adjustments were required in some cases. One patient developed mild thrombocytopenia. Abrocitinib demonstrated rapid, significant clinical improvement and was generally well-tolerated, supporting its role as an effective option for moderate-to-severe AD, particularly in patients with inadequate response to cyclosporine.

Ruxolitinib (RUX) cream 1.5%, a selective Janus kinase (JAK) 1 and 2 inhibitor initially developed for myelofibrosis, has emerged as a novel therapeutic agent in dermatology. It is the first topical JAK inhibitor approved by the Food and Drug Administration for atopic dermatitis (AD) and non-segmental vitiligo. This article reviews the pharmacological profile, mechanism of action, and clinical efficacy of topical RUX in immune-mediated skin conditions. RUX inhibits cytokine-induced JAK-signal transducer and activator of transcription signaling, reducing inflammation and pruritus with minimal systemic absorption and a favorable safety profile. In phase III TRuE-AD1/AD2 trials, RUX demonstrated significant improvements in the investigator’s global assessment, eczema area and severity index scores, and pruritus in patients with mild-to-moderate AD. Similarly, in the TRuE-V1/V2 studies for vitiligo, RUX achieved superior rates of facial vitiligo area scoring index (F-VASI75) and other repigmentation measures compared to vehicle, with sustained benefits at week 52. Common adverse effects included application site reactions such as burning, acne, and pruritus. Beyond its approved indications, emerging evidence supports off-label use in conditions such as lichen planus, alopecia areata, and cutaneous lupus, among others. While preliminary data suggest a positive impact on the skin microbiome, further studies are warranted. RUX cream represents a promising advancement in targeted dermatological therapy, offering localized efficacy with minimal systemic risk.

Omalizumab, an anti-IgE monoclonal antibody, is a standard treatment for chronic spontaneous urticaria (CSU). In India, an ‘intended-copy biosimilar’ (ICB) was introduced in 2020, based on structural similarity, without clinical trials. This case series compares the efficacy and safety of ICBs with the original biologic. A retrospective review of nine patients with CSU (mean age 37.1 years) who switched from omalizumab to an ICB due to the unavailability of omalizumab. Disease control was assessed using the Urticaria Activity Score and the Urticaria Control Test. Findings highlight the need for rigorous biosimilar testing and standardized nomenclature to distinguish biosimilar types.