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Aims/Introduction  Dipeptidyl peptidase‐4 inhibitor has been proven to improve glycemic control and β‐cell function in latent autoimmune diabetes in adults ( LADA ). The potential immune modulation mechanism is still unknown. Thus, we tested T‐lymphocyte subsets and expression of relevant transcription factors in  LADA  patients with sitagliptin intervention for up to 1‐year.    Materials and Methods  A total of 40  LADA  patients were randomly assigned to sitagliptin and/or insulin treatment ( SITA  group;  n  = 20) or insulin alone treatment ( CONT  group;  n  = 20). Peripheral blood mononuclear cells were isolated at baseline, 6 months and 12 months. The percentage of T‐lymphocyte subsets (T helper 1, T helper 2, T helper 17 and regulatory T cells) tested by flow cytometry, and the messenger ribonucleic acid expression (T box expressed in T cells [T‐BET],  GATA  binding protein 3 [GATA3], forkhead box protein 3 [FOXP3] and related orphan receptor C [ RORC ]) tested by real‐time polymerase chain reaction were determined at baseline, 6 months and 12 months.    Results  The percentage of regulatory T cells in the  SITA  group was significantly lower than that of the  CONT  group at baseline. The percentage of T helper 2 cells was higher than that of the  CONT  group at 6 months and 12 months. At 12 months, the percentage of T helper 17 cells was lower in the  SITA  group than that of the  CONT  group. After a 1‐year visit, the messenger ribonucleic acid expression levels of T‐BET expressed in T cells and  RORC  in the  SITA  group were significantly lower than at baseline. Whereas that of  RORC  in the  CONT  group were significantly lower than that at baseline.    Conclusions  The data confirmed that sitagliptin altered the phenotype of T cells and downregulated the expression of T‐BET and  RORC  in  LADA  patients, and ameliorated glycemic control in  LADA  patients.

journal of diabetes investigation

Altered T‐cell subsets and transcription factors in latent autoimmune diabetes in adults taking sitagliptin, a dipeptidyl peptidase‐4 inhibitor: A 1‐year open‐label randomized controlled trial