Psoriatic arthritis from pathogenesis to therapy 英文参考文献.docVIP

Available online /content/11/1/214 Review Psoriatic arthritis: from pathogenesis to therapy Oliver FitzGerald1 and Robert Winchester2 1Department of Rheumatology, St Vincent’s University Hospital, Elm Park, Dublin, 4, Ireland 2Department of Medicine, Division of Rheumatology, Columbia University, New York, NY 10032, USA Corresponding author: Oliver FitzGerald, oliver.fitzgerald@ucd.ie Published: 12 February 2009 Arthritis Research Therapy 2009, 11:214 (doi:10.1186/ar2580) This article is online at /content/11/1/214 ? 2009 BioMed Central Ltd Abstract [2]; and the response to therapeutic agents directed at activated T cells (for example, DAB389IL-2 or alefacept), as well as to effector pathways resulting from T-cell activation. Autoantibodies are not detectable in PsA, distinguishing this and the other class I associated diseases, such as ankylosing spondylitis, from the autoimmune diseases associated with class II MHC alleles, in which autoantibodies presumably engendered through CD4+ T-cell help are conspicuous. As is the case with all autoimmune diseases, the nature of the peptide that drives the T-cell response remains unknown, and some of the reasons for the difficulty of this identification in PsA are mentioned. Psoriatic arthritis is a multigenic autoimmune disease that involves synovial tissue, entheseal sites and skin, and that may result in signi- ficant joint damage. Although there are no diagnostic tests for psoriatic arthritis, research has identified consistent features that help to distinguish the condition from other common rheumatic diseases. Comparison of HLA-B and HLA-C regions in psoriatic arthritis with those in psoriasis without joint involvement demon- strates significant differences, such that psoriatic arthritis cannot be viewed simply as a subset of genetically homogeneous psoriasis. T- cell receptor phenotypic studies have failed