title: TNF-like ligand 1A is associated with the pathogenesis of psoriasis vulgaris and contributes to IL-17 production in PBMCs.
abstract: TNF-like ligand 1A (TL1A), a newly identified member of the TNF superfamily, has been proved as an important mediator of inflammation and critically involved in the pathogenesis of rheumatoid arthritis and several other autoimmune diseases. The aim of our study was to determine the possible role of TL1A in the pathogenesis of psoriasis. In this study, serum levels of TL1A in patients with psoriasis vulgaris (PV) and atopic dermatitis (AD) were detected by enzyme-linked immunosorbent assay (ELISA). Then, peripheral blood mononuclear cells (PBMCs) from patients with PV were isolated, the mRNA expression of TL1A was measured by real-time quantitative PCR. The effects of TL1A on the production of T cell cytokines, such as IL-17, IFN-γ, IL-4 and IL-10 in PBMCs were determined. We demonstrated that serum TL1A levels were significantly elevated in patients with PV but not in patients with AD. Besides, the high serum TL1A levels in patients with PV decreased after treatment. PBMCs derived from psoriatic patients showed significantly increased TL1A mRNA levels. Soluble TL1A synergized with IL-23 to stimulate PBMCs from patients with PV to produce IL-17. Taken together, these findings strongly suggest that TL1A may play a role in the pathogenesis of PV.
authors.affiliation: Department of Dermatovenereology, Chengdu Second People's Hospital, No. 165, Caoshi Street, Chengdu, 610017, Sichuan, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Li
authors.forename: Lixin
authors.initials: L
authors.lastname: Fu
authors.forename: Yonghong
authors.initials: Y
authors.lastname: Lu
authors.forename: Wenju
authors.initials: W
authors.lastname: Wang
authors.forename: Hui
authors.initials: H
authors.lastname: Liu
authors.forename: Fang
authors.initials: F
authors.lastname: Li
authors.forename: Tao
authors.initials: T
authors.lastname: Chen
mesh_terms: D000293:Adolescent; D000328:Adult; D016022:Case-Control Studies; D002478:Cells, Cultured; D002648:Child; D003876:Dermatitis, Atopic / Q000276:immunology / Q000378:metabolism; D005260:Female; D006801:Humans; D020381:Interleukin-17 / Q000276:immunology / Q000378:metabolism*; D053759:Interleukin-23 / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D011565:Psoriasis / Q000097:blood / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000628:therapy; D012333:RNA, Messenger / Q000378:metabolism; D015398:Signal Transduction; D053380:Tumor Necrosis Factor Ligand Superfamily Member 15 / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D020381:Interleukin-17; D053759:Interleukin-23; D012333:RNA, Messenger; C117026:TNFSF15 protein, human; D053380:Tumor Necrosis Factor Ligand Superfamily Member 15