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脂肪细胞和内皮细胞来源的介质对免疫细胞细胞因子产生的偏斜。

Skewing of immune cell cytokine production by mediators from adipocytes and endothelial cells.

机构信息

Department of Otolaryngology; Medical University of South Carolina; Charleston, SC USA ; Department of Clinical Microbiology and Parasitology; University of Los Andes; Merida, Venezuela.

Research Service; Ralph H. Johnson VA Medical Center; Charleston, SC USA ; Department of Medicine; Division of Endocrinology, Diabetes and Genetic Medicine; Medical University of South Carolina; Charleston, SC USA.

出版信息

Adipocyte. 2014 Apr 1;3(2):126-31. doi: 10.4161/adip.28287. Epub 2014 Feb 25.

DOI:10.4161/adip.28287
PMID:24719786
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3979877/
Abstract

Since adipose tissue is composed of adipocytes as well as other cell types including endothelial cells, this study sought to determine how mediators from adipocytes and from endothelial cells impact on immune cell production of cytokines. A minimalistic design was used in which media conditioned by adipocytes or by endothelial cells were added individually or as a mixture to normal spleen cells. Media from adipocytes or endothelial cells each stimulated spleen cell production of Th1 cytokines, Th2 cytokines, most of the measured inflammatory cytokines, and some chemokines. However, a mixture of media conditioned by adipocytes and by endothelial cells inhibited production of Th1 cytokines and skewed reactivity toward a Th2 and inflammatory phenotype. Adiponectin, but not leptin, was shown to contribute to the skewing of immune responsiveness to endothelial cell-derived mediators.

摘要

由于脂肪组织由脂肪细胞以及其他细胞类型组成,包括内皮细胞,因此本研究旨在确定脂肪细胞和内皮细胞来源的介质如何影响免疫细胞细胞因子的产生。采用了极简设计,单独或混合添加由脂肪细胞或内皮细胞条件化的培养基至正常脾细胞中。来自脂肪细胞或内皮细胞的培养基均刺激脾细胞产生 Th1 细胞因子、Th2 细胞因子、大多数测量的炎性细胞因子和一些趋化因子。然而,由脂肪细胞和内皮细胞条件化的培养基混合物抑制 Th1 细胞因子的产生,并使反应偏向 Th2 和炎症表型。结果表明,脂联素而非瘦素有助于免疫反应对内皮细胞衍生介质的偏向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e55a/3979877/0b4aec3e4346/adip-3-126-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e55a/3979877/8cd9b04926c1/adip-3-126-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e55a/3979877/f9c43e760c8a/adip-3-126-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e55a/3979877/8d5f7aa06519/adip-3-126-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e55a/3979877/a31b1298039a/adip-3-126-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e55a/3979877/0b4aec3e4346/adip-3-126-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e55a/3979877/8cd9b04926c1/adip-3-126-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e55a/3979877/f9c43e760c8a/adip-3-126-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e55a/3979877/8d5f7aa06519/adip-3-126-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e55a/3979877/a31b1298039a/adip-3-126-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e55a/3979877/0b4aec3e4346/adip-3-126-g5.jpg

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