Previously we reported that CXCL10 in type 1 diabetes (T1D) is higher than controls, and the level reflects islet associated antigen specific T cell responses and disease activity in T1D (Diabetes Care, 2001). However, little is known regarding the relationship between CXCL10 level and autoantibody levels in T1D. Therefore, we investigated relationship between the marker of cellular immunity including CXCL10 levels and islet associated autoantibody levels in T1D. We obtained informed consent and blood samples from 101 T1D patients, and examined HLA (DRB1*04:05, *09:01; susceptible HLA types in Japanese), serum CXCL10, insulin peptide (B9-23, 10-24, 11-25, 12-26) and PPD reactive T cell responses by using ELISPOT (IFNg), GAD, IA-2, ZnT8 Abs and insulin antibody. Because it has been reported that BCG administration might affect the autoimmune responses in T1D, we assessed the PPD responses in these patients as well. Among them, we focused to GAD Ab positive T1D including acute onset (n=28, 13 male and 15 female, mean age 43.1 years, disease duration 5.9 years), and slowly progressive type (n=17, 9 male and 8 female, mean age 56.9 years, disease duration 9.1 years); i.e., autoimmune diabetes subjects. We found significant positive correlation between serum CXCL10 and insulin antibody levels in the autoimmune diabetes with DRB1*09:01 (p<0.05), but it was not the case in those with DRB1*04:05. Interestingly, there was significant positive correlation between insulin peptide reactive T cells and PPD responses in the autoimmune diabetes with DRB1 09:01 (p<0.05), but it was not the case in those with DRB1 04:05. The observation was still true when we focused to acute onset subjects. These results suggest that insulin antibody levels seem to reflect higher disease activity in the autoimmune diabetes with DR9, and modulation of PPD responses may affect insulin peptide T cell responses in those patients.


A. Shimada: Advisory Panel; Self; Terumo Medical Corporation. Speaker's Bureau; Self; Abbott, Eli Lilly and Company, Novo Nordisk A/S, Sanofi-Aventis. A. Satomura: None. A. Haisa: None. Y. Oikawa: None.

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