The resident immune population of pancreatic islets has roles in islet development, beta cell physiology, and the pathology of diabetes. These roles have largely been attributed to islet macrophages, comprising 90% of islet immune cells (in the absence of islet autoimmunity), and, in the case of type 1 diabetes, to infiltrating autoreactive T cells. In adipose, tissue-resident and recruited T and B cells have been implicated in the development of insulin resistance during diet-induced obesity and ageing, but whether this is paralleled in the pancreatic islets is not known. Here, we investigated the non-macrophage component of resident islet immune cells in islets isolated from C57BL/6 J male mice during ageing (3 to 24 months of age) and following similar weight gain achieved by 12 weeks of 60% high fat diet. Immune cells were also examined by flow cytometry in cadaveric non-diabetic human islets. Immune cells comprised 2.7 ± 1.3% of total islet cells in non-diabetic mouse islets, and 2.3 ± 1.7% of total islet cells in non-diabetic human islets. In 3-month old mice on standard diet, B and T cells each comprised approximately 2–4% of the total islet immune cell compartment, and approximately 0.1% of total islet cells. A similar amount of T cells were present in non-diabetic human islets. The majority of islet T cells expressed the αβ T cell receptor, and were comprised of CD8-positive, CD4-positive, and regulatory T cells, with a minor population of γδ T cells. Interestingly, the number of islet T cells increased linearly (R2 = 0.9902) with age from 0.10 ± 0.05% (3 months) to 0.38 ± 0.11% (24 months) of islet cells. This increase was uncoupled from body weight, and was not phenocopied by a degree similar weight gain induced by high fat diet in mice. This study reveals that T cells are a part of the normal islet immune population in mouse and human islets, and accumulate in islets during ageing in a body weight-independent manner. Though comprising only a small subset of the immune cells within islets, islet T cells may play a role in the physiology of islet ageing.

中文翻译：

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T细胞在衰老过程中在非糖尿病胰岛中积累

胰岛的常驻免疫种群在胰岛发育，β细胞生理和糖尿病病理中具有作用。这些作用主要归因于胰岛巨噬细胞，包括90％的胰岛免疫细胞（在没有胰岛自身免疫的情况下），以及在1型糖尿病的情况下，归因于自身反应性T细胞的浸润。在脂肪中，在饮食诱导的肥胖和衰老过程中，组织驻留的和募集的T细胞和B细胞与胰岛素抵抗的发展有关，但是在胰岛中是否平行尚不清楚。在这里，我们研究了从C57BL / 6 J雄性小鼠的衰老过程（3至24个月大）中分离出的胰岛中常驻胰岛免疫细胞的非巨噬细胞成分，以及60％高脂饮食12周后实现的类似体重增加。还通过流式细胞术检查了尸体非糖尿病人胰岛中的免疫细胞。在非糖尿病小鼠胰岛中，免疫细胞占总胰岛细胞的2.7±1.3％，在非糖尿病人胰岛中占总胰岛细胞的2.3±1.7％。在3个月大的标准饮食小鼠中，B和T细胞分别占胰岛免疫细胞总数的2-4％，约占胰岛细胞总数的0.1％。非糖尿病人胰岛中存在相似量的T细胞。大部分胰岛T细胞表达αβT细胞受体，并且由CD8阳性，CD4阳性和调节性T细胞组成，而少数是γδT细胞。有趣的是，随着年龄的增长，胰岛T细胞的数量从0.10±0.05％（3个月）线性增加（R2 = 0.9902）到0.38±0.11％（24个月）。这种增加与体重无关，并且没有被高脂饮食在小鼠中引起的相似程度的体重增加表型化。这项研究表明，T细胞是小鼠和人类胰岛中正常胰岛免疫种群的一部分，并且在衰老过程中以不依赖体重的方式积累在胰岛中。尽管胰岛T细胞仅包含一小部分免疫细胞，但可能在胰岛衰老的生理过程中起作用。