Table 1.
Key Findings | Major Methodologies | |
---|---|---|
A role of skin TRM in protective immunity in humans | FACS | [58] |
Skin TRM with the potential of producing cytokines are infiltrated in the lesion of patients with GVHD | FC, single-cell TCR sequencing, and IF | [46] |
Cells residing in nonlesional skin are sufficient, and the recruitment of circulating cells is not necessary for the development of psoriatic disease | Transplantation, FC, quantitative RT-PCR, and IHC | [76] |
CD8+ TRM producing IL-17A in the epidermis is one of the characteristics in psoriasis | FC and IHC | [87] |
The increase in IL-17A-producing CD8+ TRM during the distribution of IFN-γ-producing TRM occurs according to psoriasis duration | FC and IF | [88] |
The successful treatment with IL-17A-targeting biologics results in a decreased number of IL-17A-producing CD8+ TRM in resolved psoriatic skin, but the frequency of these cells is not altered | FC, IHC, and IF | [91] |
IL-17A-producing CD8+ TRM and IL-22-producing CD4+ TRM remain in the psoriatic epidermis for as long as six years after starting the successful TNF-α-targeting treatment | FC, quantitative RT-PCR, and IF | [62] |
FC: flow cytometry, TCR: T-cell receptor, RT-PCR: reverse transcription polymerase chain reaction, IF: immunofluorescence, IHC: immunohistochemistry.