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来自乙型肝炎相关肝衰竭患者的肝肌成纤维细胞可能通过前列腺素E2调节自然杀伤细胞功能。

Liver myofibroblasts from hepatitis B related liver failure patients may regulate natural killer cell function via PGE2.

作者信息

Zhang Min, Wang Fenglan, Chong Yutian, Tai Qiang, Zhao Qiyi, Zheng Yubao, Peng Liang, Lin Shumei, Gao Zhiliang

机构信息

Department of Infectious Diseases, Third Affiliated Hospital of Sun Yat-sen University, No. 600 Tianhe Road, Guangzhou, 510630, Guangdong Province, China.

Department of Infectious Diseases, First Affiliated Hospital of Medical College of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, 710061, Shanxi Province, China.

出版信息

J Transl Med. 2014 Nov 4;12:308. doi: 10.1186/s12967-014-0308-9.

DOI:10.1186/s12967-014-0308-9
PMID:25367326
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4232720/
Abstract

BACKGROUND

Natural killer (NK) cells are abundant in the liver and constitute a major innate immune component that contributes to immune-mediated liver injury. However, few studies have investigated the phenotypes and functions of NK cells involved in hepatitis B related liver failure (LF), and the precise mechanism underlying NK cell regulation is not fully understood.

METHODS

We detected the percentage and function of peripheral NK cells both in hepatitis B related LF patients and healthy volunteers by flow cytometry and isolated the liver myofibroblasts (LMFs) from hepatitis B related LF livers. To determine the possible effects of LMFs on NK cells, mixed cell cultures were established in vitro.

RESULTS

We found a down-regulated percentage of peripheral NK cells in hepatitis B related LF patients, and their NK cells also displayed decreased activated natural cytotoxicity receptors (NCRs) and cytokine production. In a co-culture model, LMFs sharply attenuated IL-2-induced NK cell triggering receptors, cytotoxicity, and cytokine production. The inhibitory effect of LMFs on NK cells correlated with their ability to produce prostaglandin (PG) E2.

CONCLUSION

These data suggest that LMFs may protect against immune-mediated liver injury in hepatitis B related LF patients by inhibiting NK cell function via PGE2.

摘要

背景

自然杀伤（NK）细胞在肝脏中含量丰富，是先天性免疫的主要组成部分，参与免疫介导的肝损伤。然而，很少有研究调查参与乙型肝炎相关肝衰竭（LF）的NK细胞的表型和功能，NK细胞调节的确切机制尚未完全阐明。

方法

我们通过流式细胞术检测了乙型肝炎相关LF患者和健康志愿者外周血NK细胞的百分比和功能，并从乙型肝炎相关LF肝脏中分离出肝肌成纤维细胞（LMF）。为了确定LMF对NK细胞的可能影响，我们在体外建立了混合细胞培养体系。

结果

我们发现乙型肝炎相关LF患者外周血NK细胞百分比下调，其NK细胞还表现出活化的自然细胞毒性受体（NCR）和细胞因子产生减少。在共培养模型中，LMF显著减弱了IL-2诱导的NK细胞触发受体、细胞毒性和细胞因子产生。LMF对NK细胞的抑制作用与其产生前列腺素（PG）E2的能力相关。

结论

这些数据表明，LMF可能通过PGE2抑制NK细胞功能，从而保护乙型肝炎相关LF患者免受免疫介导的肝损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6311/4232720/abab898f1e52/12967_2014_308_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6311/4232720/15e0e17c68a5/12967_2014_308_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6311/4232720/4a0d30495662/12967_2014_308_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6311/4232720/fbe9aa66d73e/12967_2014_308_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6311/4232720/abab898f1e52/12967_2014_308_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6311/4232720/15e0e17c68a5/12967_2014_308_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6311/4232720/4a0d30495662/12967_2014_308_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6311/4232720/fbe9aa66d73e/12967_2014_308_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6311/4232720/abab898f1e52/12967_2014_308_Fig4_HTML.jpg

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