Ge Gai, Shang Jingzhe, Gan Tian, Chen Zhiming, Pan Chun, Mei Youming, Long Siyu, Wu Aiping, Wang Hongsheng
Laboratory of Mycobacteria, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, People's Republic of China.
Center for Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, People's Republic of China.
J Inflamm Res. 2023 Jun 14;16:2521-2533. doi: 10.2147/JIR.S407650. eCollection 2023.
Psoriasis (Ps) and leprosy are chronic inflammatory skin disorders, characterised by enhanced innate and adaptive immunity. Ps and leprosy rarely coexist. The molecular immune mechanism of the Ps and leprosy rarely coexistence is unclear.
RNA-sequencing (RNA-seq) was performed on 20 patients with Ps, 5 adults with lepromatous leprosy (L-lep), and 5 patients with tuberculoid leprosy (T-lep) to analyse the differentially expressed genes (DEGs) between them. Moreover, the biological mechanism of Ps and leprosy was explored by Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, Gene Ontology (GO) analysis, Gene Set Enrichment Analysis analysis, and protein-protein interaction (PPI) analyses. Finally, 13 DEGs of 10 skin biopsies of Ps patients, 6 samples of L-lep patients, 6 samples of T-lep patients and 5 healthy controls were confirmed by quantitative real-time polymerase chain reaction (qRT-PCR).
The PPI network was constructed and primarily associated with immune response, IL-17 signalling, and Toll-like receptor pathway between Ps and leprosy. Th17 markers (interleukin ()-, and () had higher expression in Ps than in L-lep and T-lep, whereas macrophage biomarkers ( and , and dendritic cell (DC)-related hallmarks () and had significantly lower expression across Ps and T-lep than in L-lep.
To put it simply, Ps patients with , and in conjunction with with up-graduated expression might be not susceptible to L-lep. However, high levels of , and in L-lep patients indicated that they unlikely suffered from Ps.
银屑病（Ps）和麻风是慢性炎症性皮肤病，其特征为固有免疫和适应性免疫增强。Ps和麻风很少共存。Ps与麻风很少共存的分子免疫机制尚不清楚。
对20例Ps患者、5例成人瘤型麻风（L-lep）患者和5例结核样型麻风（T-lep）患者进行RNA测序（RNA-seq），以分析它们之间的差异表达基因（DEG）。此外，通过京都基因与基因组百科全书（KEGG）分析、基因本体论（GO）分析、基因集富集分析和蛋白质-蛋白质相互作用（PPI）分析来探索Ps和麻风的生物学机制。最后，通过定量实时聚合酶链反应（qRT-PCR）对10例Ps患者皮肤活检样本、6例L-lep患者样本、6例T-lep患者样本和5例健康对照的13个DEG进行验证。
构建了PPI网络，其主要与Ps和麻风之间的免疫反应、IL-17信号传导和Toll样受体途径相关。Th17标志物（白细胞介素（）-和（）在Ps中的表达高于L-lep和T-lep，而巨噬细胞生物标志物（和，以及树突状细胞（DC）相关标志物（）和在Ps和T-lep中的表达均显著低于L-lep。
简而言之，具有、和且表达上调的Ps患者可能不易患L-lep。然而，L-lep患者中高水平的、和表明他们不太可能患Ps。
