# Possible Involvement of Skin‐Resident Memory T Cells in Refractory Chronic Alopecia Areata

## TL;DR

This study explores the role of skin-resident memory T cells in chronic alopecia areata and suggests JAK inhibitors may help treat resistant cases.

## Contribution

The study identifies a potential link between skin TRM cells and treatment resistance in chronic alopecia areata.

## Key findings

- CD8+CD103+ T and CD69+CD103+ T cells increase with disease duration and refractoriness in alopecia areata.
- JAK inhibitors reduced CD103+ cell infiltration in a treatment-resistant alopecia areata case.
- Skin TRM cells may contribute to the chronicity and resistance of alopecia areata.

## Abstract

Alopecia areata is a typical skin disease with unmet needs. So far, it has been understood that the main cause of the intractability of chronic cases is the decrease in inflammatory cell infiltration and falling into the telogen‐like phase. However, in some cases, even in long‐term chronic cases, inflammatory cell infiltration can be seen, so that we speculate that the long‐term persistence of these perifollicular cells may be the reason for the lack of improvement as skin resident memory T (TRM) cells. To investigate the presence of TRM, nine treatment‐resistant chronic AA patients and 5 acute AA patients were employed for staining with CD69 and CD103 as markers for identifying skin TRM cells. This study revealed the number of CD8+CD103+ T and CD69+CD103+ T cells tended to increase with increasing disease duration and refractoriness. In one case of AA refractory to conventional treatment, an oral JAK inhibitor (JAKi) showed dramatic efficacy with a reduction in the number of infiltrating CD103+ cells, including CD8+CD103+ T and CD69+CD103+ T cells. These results suggest that refractory cases in the chronic phase tend to have more infiltrating skin TRM cells, and JAKi may be effective in the refractory cases of chronic AA.