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The following is a summary of “FC02 Immune cell signatures and T-cell receptor profiling reveal pathogenetic mechanisms in psoriasis,” published in the December 2024 issue of Dermatology by Deng et al.
Researchers conducted a retrospective study to investigate the immune response associated with psoriasis and gain better insights into its underlying mechanisms.
They performed single-cell RNA sequencing and parallel single-cell T-cell receptor (TCR) profiling on peripheral blood mononuclear cells collected from 11 patients with psoriasis and 8 healthy controls. Additionally, 2 pairs of skin samples from the psoriasis group were analyzed, and spatial transcriptomics was conducted on 2 other pairs of skin samples.
The results showed distinct immune signatures in myeloid and lymphocyte subsets in both blood and skin in psoriasis. An increased proportion of circulating CD14+ monocytes were identified. Plasmacytoid dendritic cells in patients with psoriasis displayed elevated expression of genes linked to skin-homing and pro-inflammatory responses. Circulating T cells exhibited reduced activation marker expression. In psoriatic lesions, resting CD8+ tissue-resident memory T (TRM) cells showed gene expression similar to activated CD8+ TRM cells but with lower cytotoxicity-related gene expression. Both resting and activated CD8+ TRM cells in lesions had stronger signal transmission and reception compared to non-lesions. Activated CD8+ TRM cells were more densely infiltrated in dermal skin lesions while resting CD8+ TRM cells were located deeper in the non-lesion dermis. The TCR clones highly expanded in lesions were mainly CD8+ TRM cells. Different TCR clusters displayed varied gene expressions, with 1 cluster expressing IFNγ and another expressing IL-17.
Investigators concluded valuable insights into immune cell dynamics in both circulation and local skin environments, contributing to the understanding of psoriasis pathogenesis.
Source: academic.oup.com/bjd/article/191/Supplement_3/ljae360.002/7916084
