title: Th17 Cells in Immunopathogenesis and treatment of rheumatoid arthritis.
abstract: Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by the sequestration of various leukocyte subpopulations within both the developing pannus and synovial space. The chronic nature of this disease results in inflammation of multiple joints, with subsequent destruction of the joint cartilage and erosion of bone. Identification of T helper (Th)17 cells led to breaking the dichotomy of the Th1/Th2 axis in immunopathogenesis of autoimmune diseases such as RA, and its experimental model, collagen-induced arthritis (CIA). Th17 cells produce cytokines, including interleukin (IL)-17, IL-6, IL-21, IL-22 and tumor necrosis factor (TNF)-α, with pro-inflammatory effects, which appear to have a role in immunopathogenesis of RA. Regarding the wide ranging production of pro-inflammatory cytokines and chemokines by Th17 cells, it is expected that Th17 cell could be a potent pathogenic factor in disease immunopathophysiology. Thus the identification of effector mechanisms used by Th17 cells in induction of disease lesions may open new prospects for designing a new therapeutic strategy for treatment of RA.
authors: Imam Hassan Mojtaba Hospital, Alborz University of Medical Sciences, Karaj, Iran.
authors: Gholamreza
authors: G
authors: Azizi
authors: Farhad
authors: F
authors: Jadidi-Niaragh
authors: Abbas
authors: A
authors: Mirshafiey
mesh_terms: D000818:Animals; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000175:diagnosis / Q000188:drug therapy* / Q000276:immunology; D016207:Cytokines / Q000378:metabolism*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D007596:Joints / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D015398:Signal Transduction / Q000187:drug effects; D058504:Th17 Cells / Q000187:drug effects* / Q000276:immunology; D016896:Treatment Outcome
chemical_list: D018501:Antirheumatic Agents; D016207:Cytokines; D018836:Inflammation Mediators
keywords: IL‐17; RA; Th17; immunopathogenesis; rheumatoid arthritis