Nicotine- and tar-removed cigarette smoke extract modulates the antigen presentation function of mouse bone marrow-derived dendritic cells

IF 1.9 4区 医学 Q4 IMMUNOLOGY
Kazuyuki Furuta, Takehiro Yoshioka, Kana Nishikaze, Noriko Yoshikawa, Kazuki Nakamura, Chikara Kaito
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Abstract

Dendritic cells (DCs) take up antigens derived from pathogens such as bacteria and viruses, and from tumor cells and induce the activation of antigen-specific T cells through major histocompatibility complex (MHC)-mediated antigen presentation. Mainstream cigarette smoke extract (CSE) has various effects, and the effects of its major components, nicotine and tar, have been analyzed extensively. Recently, the physiological effects of nicotine- and tar-removed CSE (cCSE) have also been reported. However, the effects of cCSE on DC-mediated immune responses remain unknown. In this study, we found that cCSE enhanced lipopolysaccharide (LPS)-stimulated induction of the expression of MHC-I and MHC-II on the cell surface of mouse bone marrow-derived DCs (BMDCs). In contrast, cCSE suppressed the induction of CD86 induced by stimulation with curdlan and interferon-γ (IFN-γ). In addition, cCSE suppressed the production of IL-12, IL-23, and IL-10 by LPS and curdlan stimulation. In the presence of cCSE, LPS-stimulated BMDCs showed enhanced activation of CD4 and CD8 T cells and increased IL-2 production from T cells by antigen presentation in a mixed-leukocyte reaction assay. In contrast, cCSE did not affect the activation of T cells by curdlan- or IFN-γ-stimulated BMDCs, and curdlan-stimulated BMDCs suppressed IL-17 production from T cells and enhanced IFN-γ production. These results suggest that cCSE has different effects on the activation signals induced by LPS, curdlan, and IFN-γ in BMDCs and modulates the antigen presentation function of BMDCs.

尼古丁和焦油去除香烟烟雾提取物调节小鼠骨髓来源树突状细胞的抗原呈递功能
树突状细胞(dc)吸收来自病原体(如细菌和病毒)和肿瘤细胞的抗原,并通过主要组织相容性复合体(MHC)介导的抗原呈递诱导抗原特异性T细胞的活化。主流香烟烟雾提取物具有多种作用,人们对其主要成分尼古丁和焦油的作用进行了广泛的分析。近年来,除尼古丁和焦油的CSE (cCSE)的生理效应也有报道。然而,cCSE对dc介导的免疫反应的影响尚不清楚。在本研究中,我们发现cCSE增强了脂多糖(LPS)刺激对小鼠骨髓源性DCs (bmdc)细胞表面MHC-I和MHC-II表达的诱导。相反,cCSE抑制curdlan和干扰素-γ (IFN-γ)刺激诱导的CD86的诱导。此外,cCSE通过LPS和curdlan刺激抑制IL-12、IL-23和IL-10的产生。在cCSE存在的情况下,lps刺激的BMDCs表现出CD4和CD8 T细胞的激活增强,并且在混合白细胞反应试验中通过抗原呈递增加T细胞的IL-2产生。相反,cCSE不影响凝血素或IFN-γ刺激的BMDCs对T细胞的激活,凝血素刺激的BMDCs抑制T细胞IL-17的产生,增强IFN-γ的产生。这些结果表明,cCSE对LPS、curdlan和IFN-γ诱导的BMDCs的激活信号有不同的影响,并调节BMDCs的抗原递呈功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Microbiology and Immunology
Microbiology and Immunology 医学-免疫学
CiteScore
5.20
自引率
3.80%
发文量
78
审稿时长
1 months
期刊介绍: Microbiology and Immunology is published in association with Japanese Society for Bacteriology, Japanese Society for Virology, and Japanese Society for Host Defense Research. It is peer-reviewed publication that provides insight into the study of microbes and the host immune, biological and physiological responses. Fields covered by Microbiology and Immunology include:Bacteriology|Virology|Immunology|pathogenic infections in human, animals and plants|pathogenicity and virulence factors such as microbial toxins and cell-surface components|factors involved in host defense, inflammation, development of vaccines|antimicrobial agents and drug resistance of microbes|genomics and proteomics.
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