Tim-3调节慢性乙型肝炎患者单核细胞诱导的炎性细胞因子表达

StephenW

Scand J Immunol. 2019 Feb 7:e12755. doi: 10.1111/sji.12755. [Epub ahead of print]
Tim-3 regulates inflammatory cytokine expression and Th17 cell response induced by monocytes from patients with chronic hepatitis B.
Wang J1, Li C1, Fu J1, Wang X1, Feng X2, Pan X1.
Author information

1
    Department of Infectious Disease, The Affiliated Hospital of Xuzhou Medical University, 99 West Huai-hai Rd, Xuzhou, China, 221002.
2
    Central Laboratory of the Affiliated Hospital of Xuzhou Medical University, 99 West Huai-hai Rd, Xuzhou, China, 221006.

Abstract

Tim-3 is expressed on monocytes/macrophages, and is involved in the regulation of inflammatory responses. The aim of this study was to determine the effect of Tim-3 on inflammatory response triggered by peripheral monocytes from patients with chronic hepatitis B (CHB). Tim-3 expression on peripheral monocytes and frequency of Th17 cells in peripheral blood mononuclear cells (PBMCs) derived from CHB patients were detected. Followed by lipopolysaccharides (LPS) activation of circulating monocytes from CHB patients, expression of inflammatory cytokines including TNF-α,IL-1β and IL-6 were examined in the presence and absence of Galectin-9 which is the ligand for Tim-3. Subsequently, after purified CD4+T cells were co-cultured with LPS-activated monocytes from CHB patients in the presence of anti-Tim-3 antibody, percentage of Th17 cells and production of IL-17 were measured. Tim-3 expression was significantly upregulated and closely correlated to the frequency of Th17 cells in patients with CHB. Expression of TNF-α,IL-1β and IL-6 increased significantly in monocytes stimulated with LPS and Galectin-9, compared to LPS stimulation alone. LPS-activated monocytes from CHB patients could drive differentiation of memory CD4+T cells to Th17 cells. However, under the blockade of Tim-3 signaling by anti-Tim-3 antibody, percentage of Th17 cells and production of IL-17 decreased significantly. Our results demonstrate that up-regulated expression of Tim-3 on circulating monocytes accelerates inflammatory response by promoting production of inflammatory cytokines and Th17 responses in CHB. This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.
KEYWORDS:

Monocyte; Th17; Tim-3; chronic hepatitis B; inflammatory reponse

PMID:
    30729555
DOI:
    10.1111/sji.12755

StephenW

Scand J Immunol。 2019年2月7日：e12755。 doi：10.1111 / sji.12755。 [印刷前的电子版]
Tim-3调节慢性乙型肝炎患者单核细胞诱导的炎性细胞因子表达和Th17细胞应答。
王J1，李C1，傅J1，王X1，冯X2，潘X1。
作者信息

1
    徐州医科大学附属医院传染病科，徐州西淮海西路99号，邮编：221002。
2
    徐州医科大学附属医院中心实验室，徐州市西海路99号，邮编：221006。

抽象

Tim-3在单核细胞/巨噬细胞上表达，并参与炎症反应的调节。本研究的目的是确定Tim-3对慢性乙型肝炎（CHB）患者外周血单核细胞引起的炎症反应的影响。检测来自CHB患者的外周血单核细胞中Tim-3的表达和外周血单核细胞（PBMC）中Th17细胞的频率。随后脂质多糖（LPS）激活来自CHB患者的循环单核细胞，在存在和不存在作为Tim-3配体的半乳糖凝集素-9的情况下检查炎性细胞因子（包括TNF-α，IL-1β和IL-6）的表达。随后，在抗Tim-3抗体存在下，将纯化的CD4 + T细胞与来自CHB患者的LPS活化的单核细胞共培养后，测量Th17细胞的百分比和IL-17的产生。 Tim-3表达显着上调，并与CHB患者Th17细胞的频率密切相关。与单独的LPS刺激相比，用LPS和半乳糖凝集素-9刺激的单核细胞中TNF-α，IL-1β和IL-6的表达显着增加。来自CHB患者的LPS活化的单核细胞可以驱使记忆CD4 + T细胞分化为Th17细胞。然而，在抗Tim-3抗体对Tim-3信号传导的阻断下，Th17细胞的百分比和IL-17的产生显着降低。我们的研究结果表明，Tim-3在循环单核细胞上的表达上调通过促进CHB中炎性细胞因子和Th17反应的产生而加速炎症反应。本文受版权保护。版权所有。

本文受版权保护。版权所有。
关键词：

单核细胞; Th17细胞;添-3;慢性乙型肝炎;炎症反应

结论：
    30729555
DOI：
    10.1111 / sji.12755