Abrocitinib Reduces Pathogenic Skin-Resident Memory T Cells in Atopic Dermatitis

A biopsy-based analysis presented at the 2026 European Academy of Dermatology and Venereology (EADV) Congress found that abrocitinib (Cibinqo; Pfizer) reduced pathogenic skin-resident memory T (TRM) cells and restored epidermal barrier integrity in patients with atopic dermatitis (AD).¹

The findings, presented as ePoster P1634, provide additional mechanistic insight into the effects of selective Janus kinase 1 (JAK1) inhibition in AD and build on previous analyses from the phase 2a JADE MOA trial examining changes in inflammatory, immune, and skin barrier biomarkers with abrocitinib treatment.^1,2

The analysis is particularly relevant as researchers increasingly investigate the potential role of TRM cells in the chronicity and recurrence of inflammatory skin disease. These cells can persist within previously affected tissue following resolution of active inflammation, providing localized immune memory capable of responding rapidly to subsequent stimulation.

Examining Abrocitinib's Effects Within the Skin

The EADV analysis, titled “Abrocitinib reduces pathogenic skin-resident memory T cells and restores barrier integrity in atopic dermatitis: a biopsy-based analysis from the JADE MOA trial,” was presented by Piccini and colleagues.^1

JADE MOA (NCT03915496) was a randomized, double-blind, placebo-controlled phase 2a trial designed to characterize the mechanism of action of abrocitinib in adults with moderate-to-severe AD.^2 Patients received abrocitinib 200 mg once daily, abrocitinib 100 mg once daily, or placebo for 12 weeks.

The previously published primary biomarker analysis included 46 patients: 14 treated with abrocitinib 200 mg, 16 with abrocitinib 100 mg, and 16 receiving placebo. Lesional skin biopsies were collected at baseline and during treatment, with nonlesional biopsies also collected for analysis.¹

The EADV 2026 analysis used biopsy-based data from JADE MOA to further examine pathogenic TRM cells and epidermal barrier integrity. Investigators reported reductions in pathogenic skin-resident memory T cells alongside restoration of barrier integrity following abrocitinib treatment.¹

These findings add another layer to the understanding of how abrocitinib may alter the underlying biology of AD beyond improvements in visible disease.

Previous JADE MOA Findings Support Mechanistic Changes

Earlier analyses from JADE MOA demonstrated significant changes across several molecular pathways associated with AD following 12 weeks of abrocitinib treatment.²

Gene expression of markers associated with inflammation, epidermal hyperplasia, and T-helper (Th)22 immune responses—including MMP-12, KRT16, S100A8, S100A9, and S100A12—decreased from baseline with abrocitinib treatment. Changes were observed as early as week 2 with the 200-mg dose and by week 4 with the 100-mg dose, with a dose-dependent pattern reported.

Treatment with abrocitinib 200 mg also significantly decreased expression of the Th2-associated biomarker CCL17 at week 12 and CCL18 at weeks 2, 4, and 12. These molecular changes occurred alongside improvements in clinical signs of AD and reductions in itch.²

Separate research using JADE MOA samples has also provided evidence that abrocitinib treatment may alter the skin microbiome. In a 2026 analysis of 43 patients, investigators observed increased microbial diversity with abrocitinib 200 mg at week 12 and dose-dependent reductions in Staphylococcus and Staphylococcus aureus abundance from week 2 through week 12.^3 Changes in microbial composition corresponded with improvements in disease severity and immune markers.

Together, these analyses provide a broader picture of the biological changes occurring during selective JAK1 inhibition, spanning inflammatory pathways, epidermal function, microbial composition, and now skin-resident memory T-cell populations.

Potential Implications for AD Disease Memory

TRM cells have emerged as an area of interest in chronic inflammatory skin diseases because they remain within tissues after an inflammatory response has subsided. In AD, persistent pathogenic immune populations may contribute to the tendency for disease to recur, including in previously affected areas.

The reduction of pathogenic TRM cells reported in the EADV analysis therefore raises questions about whether selective JAK1 inhibition could influence mechanisms involved in persistent or recurrent disease in addition to controlling active inflammation.

However, the clinical implications of these mechanistic findings remain to be determined. The EADV analysis evaluates biological changes in skin rather than demonstrating that reductions in TRM cells translate into lower relapse rates or disease modification. Additional prospective and longer-term research would be needed to establish such a relationship.

The findings nevertheless expand the mechanistic evidence surrounding abrocitinib and suggest that its effects in AD may extend across multiple components of disease biology, including inflammatory signaling, epidermal barrier abnormalities, microbial dysbiosis, and pathogenic immune memory.

References

1. Piccini I, Koudounas S, Ludwig R, et al. Abrocitinib reduces pathogenic skin-resident memory T cells and restores barrier integrity in atopic dermatitis: a biopsy-based analysis from the JADE MOA trial. ePoster P1634. Presented at: European Academy of Dermatology and Venereology Congress; September 30-October 3, 2026; Vienna, Austria. QIMA Life Sciences
2. Guttman-Yassky E, Facheris P, Gomez-Arias PJ, et al. Effect of abrocitinib on skin biomarkers in patients with moderate-to-severe atopic dermatitis. Allergy. 2024;79(5):1258-1270. doi:10.1111/all.15969. PubMed
3. Kim M, et al. Effect of abrocitinib on the skin microbiome in patients with moderate-to-severe atopic dermatitis. Allergy. Published online August 2, 2026. doi:10.1111/all.70467.