T. Jiang, A. R. Foster, A. V. Pournara, L. Steele, M. Shabbir, E. Smith, K. Evans, T. Baxter, K. Diddams, L. Wright, V. Rowe, B. Rumney, D. Baudry, A. Rose, P. Morgan, R. Maniam, K. Stewart, J. Y. W. Lee, A. Balbaa, H. Jang, M. K. Levings, R. Woolf, A. E. Pink, V. B. M. Shanmugiah, M. Haniffa, C. H. Smith, F. Capon, S. K. Mahil
While targeted therapeutics have transformed the treatment of inflammatory skin disorders, symptoms typically return upon drug withdrawal, reflecting the relapsing remitting trajectory of these conditions. The role of tissue-resident memory T (Trm) cells in recurrence is well established, but the contribution of other memory populations is poorly understood. To address this question, we investigated the immune changes underlying drug-induced remission and recurrence in atopic dermatitis (AD). We used single-cell multi-omics to profile serial blood samples (~1.3M cells; 5 timepoints over 24 weeks) and skin biopsies (spatial transcriptomics at baseline and week 12) from patients receiving an IL4R inhibitor. We found that drug-induced AD remission was preceded by an expansion of memory regulatory T cells in blood and skin. These shifts were accompanied by a rapid decrease in the abundance of blood CD103+/CD4+ ex-Trm cells recirculating from skin. Notably, the reduced frequency of ex-Trm cells was apparent after 3 days of treatment, well in advance of clinical remission. The analysis of independent patient cohorts confirmed this and showed that the decline in ex-Trm cell abundance was reversed upon disease recurrence. Thus, we uncovered early shifts in circulating memory T cells, which anticipate the resolution and return of skin inflammation in AD.