Several of the proinflammatory peptides involved in rheumatoid arthritis pathogenesis, including peptides induced downstream of tumor necrosis factor-alpha as well as the monocyte/T cell-attracting chemokines RANTES and stromal cell-derived factor (SDF)-1alpha 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.

• MeSH
• dipeptidylpeptidasa 4 chemie   metabolismus   MeSH
• inhibitory proteas MeSH
• izoenzymy MeSH
• katalytická doména MeSH
• lidé MeSH
• myši MeSH
• peptidy metabolismus   MeSH
• revmatoidní artritida enzymologie   etiologie   patologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• dipeptidylpeptidasa 4 MeSH
• inhibitory proteas MeSH
• izoenzymy MeSH
• peptidy MeSH