Breaking old paradigms: Th17 cells in autoimmune arthritis.
Aberrant helper T cell activation has been implicated in the pathogenesis of an array of autoimmune diseases. In this review, we summarize evidence that suggests the involvement of a novel T cell subset, the Th17 lineage, in rheumatoid arthritis. In particular, we focus on the role of Th17 cells in inducing and perpetuating the chronic inflammation, cartilage damage, and bone erosion that are hallmark phases of joint destruction and consider current and emerging therapies that seek to disrupt the inflammatory Th17 network and shift the immune system back towards homeostasis.
Peck
Ariana
A
Department of Pediatrics, Division of Immunology and Transplantation Biology, Stanford University School of Medicine, Stanford, CA 94305, USA. apeck@stanford.edu
Mellins
Elizabeth D
ED
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000209:etiology / Q000276:immunology* / Q000378:metabolism; D001842:Bone and Bones / Q000378:metabolism / Q000473:pathology; D002356:Cartilage / Q000378:metabolism / Q000473:pathology; D006801:Humans; D020381:Interleukin-17 / Q000276:immunology / Q000378:metabolism*; D018448:Models, Immunological; D013585:Synovitis / Q000209:etiology / Q000276:immunology / Q000378:metabolism; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology* / Q000378:metabolism
D020381:Interleukin-17