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Arthritis Research & Therapy
Published in: Arthritis Research & Therapy 6/2005

01-12-2005 | Review

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

Authors: Aleksi Sedo, Jonathan S Duke-Cohan, Eva Balaziova, Liliana R Sedova

Published in: Arthritis Research & Therapy | Issue 6/2005

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Abstract

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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Metadata
Title
Dipeptidyl peptidase IV activity and/or structure homologs: Contributing factors in the pathogenesis of rheumatoid arthritis?
Authors
Aleksi Sedo
Jonathan S Duke-Cohan
Eva Balaziova
Liliana R Sedova
Publication date
01-12-2005
Publisher
BioMed Central
Published in
Arthritis Research & Therapy / Issue 6/2005
Electronic ISSN: 1478-6362
DOI
https://doi.org/10.1186/ar1852

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