Table of Contents Author Guidelines Submit a Manuscript
Journal of Immunology Research
Volume 2016, Article ID 1858202, 6 pages
Research Article

Immunological Aspects of Fulminant Type 1 Diabetes in Chinese

1Diabetes Center, 2nd Xiangya Hospital and Institute of Metabolism and Endocrinology, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, 139 Renmin Middle Road, Changsha, Hunan 410011, China
2The Center for Medical Research, 2nd Xiangya Hospital, Central South University, 139 Renmin Middle Road, Changsha, Hunan 410011, China

Received 14 July 2015; Revised 15 January 2016; Accepted 18 January 2016

Academic Editor: Kurt Blaser

Copyright © 2016 Zhen Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Fulminant type 1 diabetes (FT1D) is a novel subtype of type 1 diabetes characterized by extremely rapid onset and complete deficiency of insulin due to the destruction of pancreatic β cells. However, the precise mechanisms underlying the etiology of this disease remain unclear. Methods. A total of 22 patients with FT1D and 10 healthy subjects were recruited. Serum antibodies to GAD, IA2, and ZnT8 in patients were tested. And peripheral T cell responses to GAD65, insulin B9–23 peptide, or C peptide were determined in 10 FT1D patients and 10 healthy controls. The mRNA levels of several related cytokines and molecules, such as IFN-γ, IL-4, RORC, and IL-17 in PBMCs from FT1D patients were analyzed by qRT-PCR. Result. We found that a certain proportion of Chinese FT1D patients actually have developed islet-related autoantibodies after onset of the disease. The GAD, insulin, or C peptide-reactive T cells were found in some FT1D patients. We also detected a significant increase for IFN-γ expression in FT1D PBMCs as compared with that of healthy controls. Conclusion. Autoimmune responses might be involved in the pathogenesis of Chinese FT1D.