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评价特发性 CD4 淋巴细胞减少症患者发生 1 型糖尿病前的细胞和体液自身免疫。

Evaluation of cellular and humoral autoimmunity before the development of type 1 diabetes in a patient with idiopathic CD4 lymphocytopenia.

机构信息

Department of Diabetes, Endocrinology and Metabolism, Tokyo, Japan.

AIDS Clinical Center, Tokyo, Japan.

出版信息

J Diabetes Investig. 2019 Jul;10(4):1108-1111. doi: 10.1111/jdi.12997. Epub 2019 Feb 25.

DOI:10.1111/jdi.12997
PMID:30588765
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6626996/
Abstract

A 64-year-old woman developed type 1 diabetes 23 years after the diagnosis of idiopathic CD4 lymphocytopenia. To investigate the etiological interaction between idiopathic CD4 lymphocytopenia and type 1 diabetes, we carried out a longitudinal analysis related to islet-specific autoimmunity. Anti-glutamic acid decarboxylase antibody had been already weakly positive for at least 16 years and started rising at 6 months before the onset of type 1 diabetes. The seroconversion of anti-insulinoma-associated antigen-2 antibody and insulin autoantibody occurred at the time of onset. The ratio of CD8/CD4 had been gradually increasing for 8 years before type 1 diabetes onset. Notably, islet-specific glucose-6-phosphatase catalytic subunit-related protein-reactive CD8 T cells were detected at type 1 diabetes onset, and the frequency was higher than that in 15 non-diabetic controls (6.75% vs 0.49 ± 0.78%, mean ± SD). The present type 1 diabetes patient, presented with idiopathic CD4 lymphocytopenia and showed an elevated number of CD8 T cells, including the islet antigen-specific CD8 T cells that might contribute to autoimmune destruction of pancreatic β-cells.

摘要

一位 64 岁女性在诊断为特发性 CD4 淋巴细胞减少症 23 年后发生 1 型糖尿病。为了研究特发性 CD4 淋巴细胞减少症与 1 型糖尿病之间的病因学相互作用,我们进行了与胰岛自身免疫相关的纵向分析。抗谷氨酸脱羧酶抗体至少已经弱阳性 16 年,并在 1 型糖尿病发病前 6 个月开始升高。抗胰岛素瘤相关抗原-2 抗体和胰岛素自身抗体的血清转化发生在发病时。CD8/CD4 的比值在 1 型糖尿病发病前 8 年内逐渐升高。值得注意的是,在 1 型糖尿病发病时检测到胰岛特异性葡萄糖-6-磷酸酶催化亚基相关蛋白反应性 CD8 T 细胞,其频率高于 15 名非糖尿病对照者(6.75%比 0.49 ± 0.78%,平均值 ± 标准差)。本 1 型糖尿病患者表现为特发性 CD4 淋巴细胞减少症,且存在数量增加的 CD8 T 细胞,包括胰岛抗原特异性 CD8 T 细胞,可能导致胰岛β细胞的自身免疫破坏。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/6626996/b840f691701f/JDI-10-1108-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/6626996/f3ab64ca080d/JDI-10-1108-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/6626996/b840f691701f/JDI-10-1108-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/6626996/f3ab64ca080d/JDI-10-1108-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aab/6626996/b840f691701f/JDI-10-1108-g002.jpg

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