Dipeptidyl peptidase IV activity and/or structure homologs: Contributing factors in the pathogenesis of rheumatoid arthritis?

被引：0
作者：
Aleksi Sedo
Jonathan S Duke-Cohan
Eva Balaziova
Liliana R Sedova
机构：
[1] Charles University,Laboratory of Cancer Cell Biology of the 1st Faculty of Medicine
[2] Prague and the Institute of Physiology,Department of Medical Oncology, Dana
[3] Academy of Sciences,Farber Cancer Institute and Department of Medicine
[4] Harvard Medical School,undefined
[5] Institute of Rheumatology,undefined
来源：
Arthritis Research & Therapy | / 7卷
关键词：
Rheumatoid Arthritis; Rheumatoid Arthritis Patient; Vasoactive Intestinal Peptide; Synovial Fibroblast; Inflame Synovium;
D O I：
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摘要：
Several of the proinflammatory peptides involved in rheumatoid arthritis pathogenesis, including peptides induced downstream of tumor necrosis factor-α as well as the monocyte/T cell-attracting chemokines RANTES and stromal cell-derived factor (SDF)-1α and the neuropeptides vasoactive intestinal peptide (VIP) and substance P, have their biological half-lives controlled by dipeptidyl peptidase IV (DPPIV). Proteolysis by DPPIV regulates not only the half-life but also receptor preference and downstream signaling. In this article, we examine the role of DPPIV homologs, including CD26, the canonical DPPIV, and their substrates in the pathogenesis of rheumatoid arthritis. The differing specific activities of the DPPIV family members and their differential inhibitor response provide new insights into therapeutic design.
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