Altered crosstalk in the dipeptidyl peptidase-4-incretin-immune system in type 1 diabetes: A hypothesis generating pilot study

András Zóka, Gábor Barna, Orsolya Hadarits, Zahra Al-Aissa, Barna Wichmann, Györgyi Muzes, Anikó Somogyi, Gábor Firneisz

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Both GLP17-36 (via GLP1 receptor) and the dipeptidyl peptidase-4 (DPP4) cleaved form of GLP1 (GLP19-36, independently of GLP1R) may modulate the response of lymphocytes to cytokine stimuli. The incretin axis, CXCR3 (receptor of DPP4 ligand cytokines CXCL9-11) expression on Tregs and hematologic parameters were assessed in 34 patients with long standing type 1 diabetes (T1DM) and in 35 healthy controls. Serum DPP4 (sDPP4) activity, plasma total GLP1 and GLP17-36 concentrations were determined. GLP19-36 concentrations were calculated. CXCR3 expression (flow cytometry) was higher on the CD25-/lowFoxp3+ than on the CD25+Foxp3+ Tregs independently from T1DM, suggesting that CD25-/lowFoxp3+ Tregs are possibly waiting for orientational chemotactic stimuli in a "standby mode". The higher sDPP4 activities in T1DM were inversely correlated with GLP17-36 levels and GLP19-36 levels directly with lymphocyte counts in controls. Our results might indicate an altered DPP4-incretin system and altered immunoregulation including a potentially dysfunctional GLP19-36 signaling in T1DM.

Original languageEnglish
Pages (from-to)667-672
Number of pages6
JournalHuman Immunology
Volume76
Issue number9
DOIs
Publication statusPublished - Sep 2015

Keywords

  • CXCR3
  • DPP4
  • GLP1
  • T
  • Type 1 diabetes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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