Abstract

Local skin memory (LSM) describes the clinical phenomenon of an accelerated and increased inflammatory allergic contact dermatitis (ACD) response upon renewed allergen exposure. This has been ascribed to the local persistence of few, but allergen‐specific, T cells. Here, firstly, we characterized effector T cells, and, subsequently, studied which of these cell populations are present at former challenge sites and might contribute to LSM. Peripheral blood T cells were stimulated with nickel sulphate. Cellular phenotypes and chemokine receptor expression profiles were analysed by FACS‐staining: CLA together with CD4/CD8, CD45R0/RA, CXCR3, CCR4, CCR6 and CCR10. Skin biopsies were taken at 0, 3 and 21 days after allergen application and analysed for the same markers. Upon nickel‐stimulation, amount of CD4+ CLA+ CD45R0+ T cells was increased. Together with CLA, CXCR3, CCR4 and, mainly, CCR10 expression was augmented. CCR6 expression was negative on CLA+ cells. In biopsies from patch tests, cellular infiltrates were present at 3 and 21 days after allergen application. Interestingly at day 21, residing cells were localized at the perivascularity and were characterized as CD4+ CD8− CCR10+ T cells. In conclusion, nickel‐activated effector T cells can be characterised as CD4+ CD8− CLA+ memory T cells. They express CXCR3, CCR4 and, in particular, CCR10. After clinical recovery from an ACD reaction, CD4+ CCR10+ memory T cells apparently reside locally. The persistence of these CCR10+ T cells, expressing the appropriate receptor of the skin specific chemokine CCL27, can explain clinically important phenomena such as LSM and flare up reactions.

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