Over the past decades, tremendous success in the treatment of psoriasis has been achieved using biologics, such as neutralizing antibodies against TNF/TNFR, IL-23, and IL-17A/IL-17RA. Although psoriatic skin lesions appear to resolve after treatment with these biologics, lesions often recur after therapy is discontinued or during therapy. Memory T cells residing in the skin have been considered as the major driver of psoriasis relapse. However, whether structural cells in the skin such as keratinocytes and fibroblasts are involved in the relapse of psoriasis is unknown. In this review, we outline the therapeutic rationale of biologics used in the treatment of psoriasis, summarize different clinical features of psoriasis relapse on the basis of preclinical and clinical data, and specifically discuss how memory T cells and structural cells in the skin are involved in psoriasis relapse. Finally, we discuss the future challenges in the basic or clinical research on psoriasis.
Keywords: AMP, antimicrobial peptides/proteins; EpSC, epithelial stem cell; FDA, Food and Drug Administration; H3K27, histone 3 lysine 27; H3K27ac, histone 3 lysine 27 acetylation; H3K4me3, histone 3 lysine 4 trimethylation; ILC3, innate lymphoid cell 3; IMQ, imiquimod; KC, keratinocyte; PGA, Physician Global Assessment; STAT3, signal transducer and activator of transcription 3; TLR, toll-like receptor; TRM, resident memory T cell; Th, T helper; Treg, regulatory T cell; hBD, human beta-defensin; mDC, myeloid dendritic cell; pDC, plasmacytoid dendritic cell.
© 2022 The Authors.