Altered systemic and intestinal IgA immune responses in individuals with type 1 diabetes

Huang, Juan, Huang, Gan, Li, Xia, Hu, Fang, Xie, Zhiguo, Xiao, Yang, Luo, Shuoming, Chao, Chen, Guo, Keyu, Wong, F. Susan ORCID: https://orcid.org/0000-0002-2812-8845, Zhou, Zhiguang and Wen, Li 2020. Altered systemic and intestinal IgA immune responses in individuals with type 1 diabetes. Journal of Clinical Endocrinology and Metabolism 105 (12) , dgaa590. 10.1210/clinem/dgaa590

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Abstract

Objective Increasing evidence supports the observation that immunoglobulin A (IgA) exerts a critical effect on the susceptibility to autoimmunity by modulating gut homeostasis and subsequent host immunity. We hypothesized that the IgA immunity is altered in individuals with type 1 diabetes. To test our hypothesis, we investigated intestinal, oral, and peripheral IgA immune responses in individuals with type 1 diabetes. Methods We collected stool, oral cavity, and blood samples from participants diagnosed with type 1 diabetes (within 1 year and more than 1 year) and healthy control individuals. Serum islet autoantibody titers were detected by radioligand assays. IgA-bound bacteria and IgA-expressing B cells were studied by flow cytometry. Oral free IgA level was measured by enzyme-linked immunosorbent assay. Serum and stool free IgA concentrations were determined by immune-turbidimetry method. Results Individuals diagnosed with type 1 diabetes within 1 year had an increased proportion of stool IgA-bound bacteria compared with healthy control individuals. The proportion of stool IgA-bound bacteria was positively associated with glutamic acid decarboxylase autoantibody titer. Moreover, individuals with a longer disease duration displayed a higher level of IgA-bound bacteria than those diagnosed within 1 year. In contrast to healthy control individuals, type 1 diabetes patients had increased serum IgA concentrations. Conclusions Individuals with type 1 diabetes display altered IgA immunity, especially increased stool IgA-bound bacteria, which is likely to contribute to β-cell autoimmunity and the disease development, and thus, might be considered as a novel therapeutic target for the treatment of type 1 diabetes.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine
Publisher:	Oxford University Press
ISSN:	0021-972X
Date of First Compliant Deposit:	6 February 2023
Date of Acceptance:	28 August 2020
Last Modified:	06 May 2023 05:53
URI:	https://orca.cardiff.ac.uk/id/eprint/136022

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