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Anti-tumor necrosis factor-alpha therapy augments dipeptidyl peptidase IV activity and decreases autoantibodies to GRP78/BIP and phosphoglucose isomerase in patients with rheumatoid arthritis.

Publication ,  Journal Article
Mavropoulos, JC; Cuchacovich, M; Llanos, C; Aguillón, JC; Gatica, H; Pizzo, SV; Gonzalez-Gronow, M
Published in: J Rheumatol
November 2005

OBJECTIVE: To assess the enzymatic activity and biochemical status of dipeptidyl peptidase IV (DPP IV), an enzyme that participates in the degradation of proinflammatory molecules, in sera from a group of patients with rheumatoid arthritis (RA; n = 15) treated with a human anti-tumor necrosis factor-a (anti-TNF-alpha) antibody (adalimumab) for 32 weeks. IgG antibody titers against chaperone Bip (GRP78), phosphoglucose isomerase (PGI), lactate dehydrogenase (LDH), fibronectin (FN), and actin were also studied. METHODS: DPP IV activity was measured in sera using Gly-Pro-p-nitroanilide as substrate. The biochemical profile of circulating DPP IV glycoforms was assessed by isoelectric focusing gel electrophoresis. All IgG autoantibody titers and their sialylation levels were determined by ELISA. RESULTS: Patients showed significant increases in serum DPP IV enzymatic activity from basal values (3.554 +/- 1.096) with respect to those obtained at 32 weeks (4.787 +/- 0.953; p < 0.05). Changes in the biochemical profile of circulating DPP IV from acidic to more neutral isoelectric point glycoforms were also seen during treatment. The elevated titers of anti-GRP78 and anti-PGI IgG observed at the beginning of treatment decreased significantly during therapy, whereas those of anti-LDH, anti-FN, and anti-actin IgG remained unchanged. At the end of treatment, sialylation levels of anti-GRP78 and anti-PGI IgG antibodies increased to nearly normal levels. The DPP IV biochemical changes were accompanied by a significant improvement of the Disease Activity Score (DAS28). CONCLUSION: The reduced activity of DPP IV along with increased titers of circulating antibodies to GRP78 and PGI may play a role in the pathogenesis of RA and can be successfully modified by administration of adalimumab.

Duke Scholars

Published In

J Rheumatol

ISSN

0315-162X

Publication Date

November 2005

Volume

32

Issue

11

Start / End Page

2116 / 2124

Location

Canada

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • N-Acetylneuraminic Acid
  • Molecular Chaperones
  • Middle Aged
  • Male
  • L-Lactate Dehydrogenase
  • Immunoglobulin G
  • Humans
  • Heat-Shock Proteins
  • Glycoproteins
 

Citation

APA
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ICMJE
MLA
NLM
Mavropoulos, J. C., Cuchacovich, M., Llanos, C., Aguillón, J. C., Gatica, H., Pizzo, S. V., & Gonzalez-Gronow, M. (2005). Anti-tumor necrosis factor-alpha therapy augments dipeptidyl peptidase IV activity and decreases autoantibodies to GRP78/BIP and phosphoglucose isomerase in patients with rheumatoid arthritis. J Rheumatol, 32(11), 2116–2124.
Mavropoulos, John C., Miguel Cuchacovich, Carolina Llanos, Juan C. Aguillón, Hector Gatica, Salvatore V. Pizzo, and Mario Gonzalez-Gronow. “Anti-tumor necrosis factor-alpha therapy augments dipeptidyl peptidase IV activity and decreases autoantibodies to GRP78/BIP and phosphoglucose isomerase in patients with rheumatoid arthritis.J Rheumatol 32, no. 11 (November 2005): 2116–24.
Mavropoulos JC, Cuchacovich M, Llanos C, Aguillón JC, Gatica H, Pizzo SV, Gonzalez-Gronow M. Anti-tumor necrosis factor-alpha therapy augments dipeptidyl peptidase IV activity and decreases autoantibodies to GRP78/BIP and phosphoglucose isomerase in patients with rheumatoid arthritis. J Rheumatol. 2005 Nov;32(11):2116–2124.

Published In

J Rheumatol

ISSN

0315-162X

Publication Date

November 2005

Volume

32

Issue

11

Start / End Page

2116 / 2124

Location

Canada

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • N-Acetylneuraminic Acid
  • Molecular Chaperones
  • Middle Aged
  • Male
  • L-Lactate Dehydrogenase
  • Immunoglobulin G
  • Humans
  • Heat-Shock Proteins
  • Glycoproteins