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树突状细胞免疫受体 2(DCIR2)缺乏症可减少肝常规树突状细胞含量,但不影响饮食诱导肥胖的进展。

Dendritic cell immunoreceptor 2 (DCIR2) deficiency decreases hepatic conventional dendritic cell content but not the progression of diet-induced obesity.

机构信息

Department of Excellence of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy.

出版信息

Immun Inflamm Dis. 2023 Oct;11(10):e1024. doi: 10.1002/iid3.1024.

DOI:10.1002/iid3.1024
PMID:37904682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10599273/
Abstract

AIMS

Inflammatory pathways and immune system dysregulation participate in the onset and progression of cardiometabolic diseases. The dendritic cell immunoreceptor 2 (DCIR2) is a C-type lectin receptor mainly expressed by conventional type 2 dendritic cells, involved in antigen recognition and in the modulation of T cell response. Here, we investigated the effect of DCIR2 deficiency during the development of obesity.

METHODS

DCIR2 KO mice and the WT counterpart were fed with high-fat diet (HFD) for 20 weeks. Weight gain, glucose and insulin tolerance were assessed, parallel to immune cell subset profiling and histological analysis.

RESULTS

After HFD feeding, DCIR2 KO mice presented altered conventional dendritic cell distribution within the liver without affecting markers of hepatic inflammation. These observations were liver restricted, since immune profile of metabolic and lymphoid organs-namely adipose tissue, spleen and mesenteric lymph nodes-did not show differences between the two groups. This reflected in a similar metabolic profile of DCIR2 KO compared to WT mice, characterized by comparable body weight gain as well as adipose tissues, spleen, Peyer's patches and mesenteric lymph nodes weight at sacrifice. Also, insulin response was similar in both groups.

CONCLUSION

Our data show that DCIR2 has a redundant role in the progression of diet-induced obesity and inflammation.

摘要

目的

炎症途径和免疫系统失调参与了心血管代谢疾病的发生和发展。树突状细胞免疫受体 2(DCIR2)是一种主要由传统 2 型树突状细胞表达的 C 型凝集素受体,参与抗原识别和 T 细胞反应的调节。在这里,我们研究了 DCIR2 缺失在肥胖发展过程中的作用。

方法

DCIR2 KO 小鼠和 WT 对照小鼠用高脂肪饮食(HFD)喂养 20 周。评估体重增加、葡萄糖和胰岛素耐量,同时进行免疫细胞亚群分析和组织学分析。

结果

在 HFD 喂养后,DCIR2 KO 小鼠肝脏内的常规树突状细胞分布发生改变,但不影响肝内炎症标志物。这些观察结果仅限于肝脏,因为代谢和淋巴器官(即脂肪组织、脾脏和肠系膜淋巴结)的免疫谱在两组之间没有差异。这反映在 DCIR2 KO 与 WT 小鼠相似的代谢特征上,表现为体重增加以及脂肪组织、脾脏、派尔氏斑和肠系膜淋巴结在处死时的重量相似。此外,两组的胰岛素反应也相似。

结论

我们的数据表明,DCIR2 在饮食诱导的肥胖和炎症的进展中具有冗余作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b3e/10599273/58e73be1e891/IID3-11-e1024-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b3e/10599273/b333da16b8b3/IID3-11-e1024-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b3e/10599273/58e73be1e891/IID3-11-e1024-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b3e/10599273/b333da16b8b3/IID3-11-e1024-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b3e/10599273/58e73be1e891/IID3-11-e1024-g003.jpg

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Inflammation in obesity, diabetes, and related disorders.肥胖、糖尿病及相关紊乱中的炎症。
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Adipose Tissue Dendritic Cells: Critical Regulators of Obesity-Induced Inflammation and Insulin Resistance.脂肪组织树突状细胞:肥胖诱导的炎症和胰岛素抵抗的关键调节者。
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