β干扰素由沙眼衣原体感染的成纤维细胞样滑膜细胞产生，并抑制γ干扰素诱导的HLA - DR表达。
Beta interferon is produced by Chlamydia trachomatis-infected fibroblast-like synoviocytes and inhibits gamma interferon-induced HLA-DR expression.
作者信息
Rödel J, Groh A, Vogelsang H, Lehmann M, Hartmann M, Straube E
机构信息
Institute of Medical Microbiology, Friedrich Schiller University of Jena, D-07743 Jena, Germany.
出版信息
Infect Immun. 1998 Sep;66(9):4491-5. doi: 10.1128/IAI.66.9.4491-4495.1998.
Abstract
Infection of fibroblast-like synovial cells with Chlamydia trachomatis (serotype D strain IC Cal 8) in culture induced the secretion of beta interferon (IFN-beta). Chlamydial infection inhibited IFN-gamma-induced expression of HLA-DR antigen in the cells. Addition of IFN-beta antibody directly to infected cultures mitigated HLA-DR inhibition, suggesting involvement of produced IFN-beta.
摘要
在培养过程中，用沙眼衣原体（血清型D株IC Cal 8）感染成纤维细胞样滑膜细胞会诱导β干扰素（IFN-β）的分泌。衣原体感染抑制了细胞中IFN-γ诱导的HLA-DR抗原表达。将IFN-β抗体直接添加到受感染的培养物中可减轻HLA-DR的抑制作用，这表明所产生的IFN-β参与其中。
相似文献
1
Beta interferon is produced by Chlamydia trachomatis-infected fibroblast-like synoviocytes and inhibits gamma interferon-induced HLA-DR expression.β干扰素由沙眼衣原体感染的成纤维细胞样滑膜细胞产生，并抑制γ干扰素诱导的HLA - DR表达。
Infect Immun. 1998 Sep;66(9):4491-5. doi: 10.1128/IAI.66.9.4491-4495.1998.
2
Role of interferon-stimulated gene factor 3gamma and beta interferon in HLA class I enhancement in synovial fibroblasts upon infection with Chlamydia trachomatis.干扰素刺激基因因子3γ和β干扰素在沙眼衣原体感染后滑膜成纤维细胞中HLA I类分子增强中的作用
Infect Immun. 2002 Nov;70(11):6140-6. doi: 10.1128/IAI.70.11.6140-6146.2002.
3
Expression of interferon regulatory factors and indoleamine 2,3-dioxygenase in Chlamydia trachomatis-infected synovial fibroblasts.沙眼衣原体感染的滑膜成纤维细胞中干扰素调节因子和吲哚胺2,3-双加氧酶的表达
Med Microbiol Immunol. 1999 May;187(4):205-12. doi: 10.1007/s004300050094.
4
Secretion of cytokines by human synoviocytes during in vitro infection with Chlamydia trachomatis.沙眼衣原体体外感染期间人滑膜细胞的细胞因子分泌
J Rheumatol. 1998 Nov;25(11):2161-8.
5
The inhibition of interferon-gamma-induced upregulation of HLA-DR expression on cultured human gingival fibroblasts by interleukin-1 beta or tumor necrosis factor-alpha.白细胞介素-1β或肿瘤坏死因子-α对干扰素-γ诱导的培养人牙龈成纤维细胞上HLA-DR表达上调的抑制作用。
J Periodontol. 1994 Apr;65(4):336-41. doi: 10.1902/jop.1994.65.4.336.
6
The role of interferon beta in human cytomegalovirus-mediated inhibition of HLA DR induction on endothelial cells.干扰素β在人巨细胞病毒介导的内皮细胞 HLA-DR 诱导抑制中的作用。
Arch Virol. 1995;140(1):111-26. doi: 10.1007/BF01309727.
7
Cytokines in chronic inflammatory arthritis. V. Mutual antagonism between interferon-gamma and tumor necrosis factor-alpha on HLA-DR expression, proliferation, collagenase production, and granulocyte macrophage colony-stimulating factor production by rheumatoid arthritis synoviocytes.慢性炎症性关节炎中的细胞因子。V. 干扰素-γ与肿瘤坏死因子-α对类风湿关节炎滑膜细胞HLA-DR表达、增殖、胶原酶产生及粒细胞巨噬细胞集落刺激因子产生的相互拮抗作用
J Clin Invest. 1990 Dec;86(6):1790-8. doi: 10.1172/JCI114908.
8
Inhibitory effect of clarithromycin on costimulatory molecule expression and cytokine production by synovial fibroblast-like cells.克拉霉素对滑膜成纤维样细胞共刺激分子表达及细胞因子产生的抑制作用。
Clin Exp Immunol. 1996 Jun;104(3):501-8. doi: 10.1046/j.1365-2249.1996.46752.x.
9
Effect of TGF-beta on interferon-gamma-induced HLA-DR expression in human retinal pigment epithelial cells.转化生长因子-β对人视网膜色素上皮细胞中干扰素-γ诱导的HLA-DR表达的影响。
Invest Ophthalmol Vis Sci. 1994 Dec;35(13):4253-9.
10
Mycobacteria inhibition of IFN-gamma induced HLA-DR gene expression by up-regulating histone deacetylation at the promoter region in human THP-1 monocytic cells.分枝杆菌通过上调人THP-1单核细胞启动子区域的组蛋白去乙酰化来抑制IFN-γ诱导的HLA-DR基因表达。
J Immunol. 2005 May 1;174(9):5687-94. doi: 10.4049/jimmunol.174.9.5687.
引用本文的文献
1
Interferon-epsilon, an estrogen-induced type I interferon, is uniquely exploited by Neisseria gonorrhoeae via effects on sialic acid metabolism.干扰素-ε是一种雌激素诱导的I型干扰素，淋病奈瑟菌通过对唾液酸代谢的影响独特地利用了它。
Cell Host Microbe. 2025 Jul 9;33(7):1133-1145.e4. doi: 10.1016/j.chom.2025.05.015. Epub 2025 Jun 9.
2
Type I IFNs contribute to upregulation of PD-L1 during infection.I型干扰素在感染期间有助于上调程序性死亡受体配体1（PD-L1）。
Infect Immun. 2025 Apr 8;93(4):e0004025. doi: 10.1128/iai.00040-25. Epub 2025 Mar 12.
3
When Bacteria and Viruses Collide: A Tale of and Sexually Transmitted Viruses.当细菌和病毒碰撞时：一个关于 和性传播病毒的故事。
Viruses. 2023 Sep 19;15(9):1954. doi: 10.3390/v15091954.
4
Modelling of Infection in the Etiopathogenesis of Male Infertility and Reactive Arthritis.感染在男性不育和反应性关节炎的病因发病机制中的作用模型。
Front Cell Infect Microbiol. 2022 Jan 31;12:840802. doi: 10.3389/fcimb.2022.840802. eCollection 2022.
5
Chlamydia trachomatis: the Persistent Pathogen.沙眼衣原体：持续性病原体
Clin Vaccine Immunol. 2017 Oct 5;24(10). doi: 10.1128/CVI.00203-17. Print 2017 Oct.
6
Analyses of the pathways involved in early- and late-phase induction of IFN-beta during C. muridarum infection of oviduct epithelial cells.在输卵管上皮细胞感染嗜肺衣原体期间，对参与IFN-β早期和晚期诱导的信号通路进行分析。
PLoS One. 2015 Mar 23;10(3):e0119235. doi: 10.1371/journal.pone.0119235. eCollection 2015.
7
Chlamydia muridarum infection associated host MicroRNAs in the murine genital tract and contribution to generation of host immune response.鼠衣原体感染相关的小鼠生殖道宿主微小RNA及其对宿主免疫反应产生的作用。
Am J Reprod Immunol. 2015 Feb;73(2):126-40. doi: 10.1111/aji.12281. Epub 2014 Jun 28.
8
Chlamydia trachomatis-infected epithelial cells and fibroblasts retain the ability to express surface-presented major histocompatibility complex class I molecules.沙眼衣原体感染的上皮细胞和成纤维细胞保留表达表面呈递的主要组织相容性复合体 I 类分子的能力。
Infect Immun. 2014 Mar;82(3):993-1006. doi: 10.1128/IAI.01473-13. Epub 2013 Dec 16.
9
STING-dependent recognition of cyclic di-AMP mediates type I interferon responses during Chlamydia trachomatis infection.STING 依赖性识别环二核苷酸介导沙眼衣原体感染期间的 I 型干扰素反应。
mBio. 2013 Apr 30;4(3):e00018-13. doi: 10.1128/mBio.00018-13.
10
Intranasal Poly-IC treatment exacerbates tuberculosis in mice through the pulmonary recruitment of a pathogen-permissive monocyte/macrophage population.鼻内 Poly-IC 治疗通过肺部募集病原体易感性单核细胞/巨噬细胞群使小鼠的结核病恶化。
J Clin Invest. 2010 May;120(5):1674-82. doi: 10.1172/JCI40817. Epub 2010 Apr 12.
本文引用的文献
1
Cellular responses to interferon-gamma.细胞对干扰素-γ的反应。
Annu Rev Immunol. 1997;15:749-95. doi: 10.1146/annurev.immunol.15.1.749.
2
Primary cultivation of human synovial cells from nonrheumatic synovial tissue and fluid.从非风湿性滑膜组织和滑液中对人滑膜细胞进行原代培养。
Exp Toxicol Pathol. 1996 Jun;48(4):243-7. doi: 10.1016/S0940-2993(96)80006-6.
3
Differential interaction with endocytic and exocytic pathways distinguish parasitophorous vacuoles of Coxiella burnetii and Chlamydia trachomatis.与内吞和外排途径的差异相互作用区分了伯纳特柯克斯体和沙眼衣原体的吞噬泡。
Infect Immun. 1996 Mar;64(3):796-809. doi: 10.1128/iai.64.3.796-809.1996.
4
Experimental Yersinia infection of human synovial cells: persistence of live bacteria and generation of bacterial antigen deposits including "ghosts," nucleic acid-free bacterial rods.人滑膜细胞的实验性耶尔森菌感染：活菌的持续存在以及包括“幽灵”（无核酸细菌杆）在内的细菌抗原沉积物的产生。
Infect Immun. 1996 Apr;64(4):1484-7. doi: 10.1128/iai.64.4.1484-1487.1996.
5
Analysis of cytokine profiles in synovial T cell clones from chlamydial reactive arthritis patients: predominance of the Th1 subset.衣原体反应性关节炎患者滑膜T细胞克隆中细胞因子谱分析：Th1亚群占优势。
Clin Exp Immunol. 1993 Oct;94(1):122-6. doi: 10.1111/j.1365-2249.1993.tb05988.x.
6
Cytokine-mediated indoleamine 2,3-dioxygenase induction in response to Chlamydia infection in human macrophage cultures.细胞因子介导的吲哚胺2,3-双加氧酶在人巨噬细胞培养物中对衣原体感染的诱导反应。
Infect Immun. 1994 Apr;62(4):1131-6. doi: 10.1128/iai.62.4.1131-1136.1994.
7
Tryptophan depletion as a mechanism of gamma interferon-mediated chlamydial persistence.色氨酸耗竭作为γ干扰素介导的衣原体持续存在的一种机制。
Infect Immun. 1994 Sep;62(9):3705-11. doi: 10.1128/iai.62.9.3705-3711.1994.
8
Antigen-presenting capacity of rheumatoid synovial fibroblasts.类风湿性滑膜成纤维细胞的抗原呈递能力。
Immunology. 1994 Jun;82(2):268-74.
9
Persistent chlamydiae: from cell culture to a paradigm for chlamydial pathogenesis.持续性衣原体：从细胞培养到衣原体发病机制的范例
Microbiol Rev. 1994 Dec;58(4):686-99. doi: 10.1128/mr.58.4.686-699.1994.
10
Zotero 插件