Psoriasis is a common, recurrent, and inflammatory skin disease (Griffiths et al., 2021). It leads to a substantial burden for individuals and society worldwide (Griffiths et al., 2021). Although IL-17 and IL-23 have been identified as key drivers of psoriasis and therapeutic targets, currently psoriasis cannot still be cured (Griffiths et al., 2021). It is necessary to explore the pathogenetic mechanisms underlying psoriasis.

Psoriasis has been considered as a T-cell driven skin disease because T helper (Th) 1 and Th17 cells are involved in psoriasis pathogenesis (Cai et al., 2013). Follicular helper T cells (TFH), mastered by transcription factor (TF) B cell lymphoma 6 (Bcl6), play an important role in germinal centers (GCs)-dependent B-cell differentiation into high-affinity antibody-producing plasma cells (PCs) (Choi and Crotty, 2021). Circulating TFH are known to be involved in numerous immune-mediated diseases. Activated circulating TFH have been reported to be associated with disease severity in patients with psoriasis (Wang et al., 2016). However, the pathological role of TFH cells in patients with psoriasis remains unknown (Niu et al., 2015).

Thus far, the pathogenetic role of B cells in psoriasis have largely been neglected (Gran et al., 2020). Elevated B lymphocytes have been shown in lesional tissue of psoriasis (Mahmoud et al., 1999). CD19+ B cell subsets in the peripheral blood and skin lesions of psoriasis patients have been reported to be correlated with disease severity (Lu et al., 2016). Moreover, autoantibodies against psoriasis autoantigens such as cathelicidin (LL-37) and melanocytic ADAMTSL5 are also strongly associated with psoriatic arthritis suggest a potential role of autoantibodies in the pathogenesis of psoriasis (Ten Bergen et al., 2020).

To explore the effect of psoriasis on B cell-mediated humoral immune response, we combined single-cell RNA-sequencing (scRNA-seq) and single-cell antigen receptor lineage (BCR)-sequencing (scBCR-seq) to generate different atlas of PBMC (Peripheral blood mononuclear cells) between healthy donors and patients with psoriasis. This would serve as a foundation for psoriasis study.