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1
The involvement of heat-shock proteins in the pathogenesis of autoimmune arthritis: a critical appraisal.热休克蛋白在自身免疫性关节炎发病机制中的作用:批判性评价。
Semin Arthritis Rheum. 2010 Oct;40(2):164-75. doi: 10.1016/j.semarthrit.2009.10.002. Epub 2009 Dec 6.
2
Self heat-shock protein 65-mediated regulation of autoimmune arthritis.自身热休克蛋白 65 介导体液性自身免疫性关节炎的调节。
J Autoimmun. 2009 Nov-Dec;33(3-4):208-13. doi: 10.1016/j.jaut.2009.09.007. Epub 2009 Oct 2.
3
Heat shock protein 65-reactive T cells are involved in the pathogenesis of non-antigenic dimethyl dioctadecyl ammonium bromide-induced arthritis.热休克蛋白65反应性T细胞参与了非抗原性二甲基二十八烷基溴化铵诱导的关节炎的发病机制。
J Immunol. 2005 Jul 1;175(1):219-27. doi: 10.4049/jimmunol.175.1.219.
4
Regulation of autoimmune arthritis by self-heat-shock proteins.自身热休克蛋白对自身免疫性关节炎的调节作用。
Trends Immunol. 2008 Sep;29(9):412-8. doi: 10.1016/j.it.2008.06.003.
5
Heat-shock proteins and autoimmunity in humans.人类中的热休克蛋白与自身免疫
Springer Semin Immunopathol. 1991;13(1):81-98. doi: 10.1007/BF01225280.
6
Heat-shock proteins as immunogenic bacterial antigens with the potential to induce and regulate autoimmune arthritis.热休克蛋白作为具有诱导和调节自身免疫性关节炎潜力的免疫原性细菌抗原。
Immunol Rev. 1991 Jun;121:5-28. doi: 10.1111/j.1600-065x.1991.tb00821.x.
7
Adjuvant arthritis and immunity to the mycobacterial 65 kDa heat shock protein.佐剂性关节炎与对分枝杆菌65 kDa热休克蛋白的免疫
Int Immunol. 1992 Jul;4(7):719-27. doi: 10.1093/intimm/4.7.719.
8
Modulation of Adjuvant Arthritis by Cellular and Humoral Immunity to Hsp65.热休克蛋白65的细胞免疫和体液免疫对佐剂性关节炎的调节作用
Front Immunol. 2016 Jun 13;7:203. doi: 10.3389/fimmu.2016.00203. eCollection 2016.
9
Antibody responses to mycobacterial and self heat shock protein 65 in autoimmune arthritis: epitope specificity and implication in pathogenesis.自身免疫性关节炎中针对分枝杆菌和自身热休克蛋白65的抗体反应:表位特异性及其在发病机制中的意义。
J Immunol. 2006 Nov 15;177(10):6634-41. doi: 10.4049/jimmunol.177.10.6634.
10
Role of the bowel flora for development of immunity to hsp 65 and arthritis in three experimental models.肠道菌群在三种实验模型中对热休克蛋白65免疫及关节炎发展的作用
Scand J Immunol. 1994 Dec;40(6):648-52. doi: 10.1111/j.1365-3083.1994.tb03518.x.

引用本文的文献

1
Autoimmunity to stromal-derived autoantigens in rheumatoid ectopic germinal centers exacerbates arthritis and affects clinical response.类风湿性异位生发中心中基质衍生自身抗原的自身免疫会加重关节炎并影响临床反应。
J Clin Invest. 2024 Apr 30;134(12):e169754. doi: 10.1172/JCI169754.
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Hsp65-Producing Prevents Antigen-Induced Arthritis in Mice.热休克蛋白 65 产生物可预防小鼠的抗原诱导性关节炎。
Front Immunol. 2020 Sep 23;11:562905. doi: 10.3389/fimmu.2020.562905. eCollection 2020.
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Heat shock protein 90α in thymic epithelial tumors and non-thymomatous myasthenia gravis.热休克蛋白 90α 在胸腺瘤和非胸腺瘤重症肌无力中的表达。
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Quantitative Proteomic Analyses To Reveal the Key Features of Proteins in New Onset Ankylosing Spondylitis Patients.定量蛋白质组学分析以揭示新发强直性脊柱炎患者蛋白质的关键特征
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Heat Shock Proteins and Inflammasomes.热休克蛋白与炎症小体。
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Serum heat-shock protein-65 antibody levels are elevated but not associated with disease activity in patients with rheumatoid arthritis and ankylosing spondylitis.类风湿关节炎和强直性脊柱炎患者血清热休克蛋白65抗体水平升高,但与疾病活动度无关。
Open Access Rheumatol. 2018 May 25;10:55-60. doi: 10.2147/OARRR.S162512. eCollection 2018.
7
Poncet's Disease in the Preclinical Phase of Rheumatoid Arthritis.类风湿关节炎临床前期的庞塞病
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8
Ras Signaling Inhibitors Attenuate Disease in Adjuvant-Induced Arthritis Targeting Pathogenic Antigen-Specific Th17-Type Cells.Ras信号抑制剂通过靶向致病性抗原特异性Th17型细胞减轻佐剂诱导性关节炎的疾病症状。
Front Immunol. 2017 Jul 7;8:799. doi: 10.3389/fimmu.2017.00799. eCollection 2017.
9
Vaccination with endosomal unknown epitopes produces therapeutic response in rheumatoid arthritis patients and modulates adjuvant arthritis of rats.用内体未知表位进行疫苗接种可使类风湿性关节炎患者产生治疗反应,并调节大鼠的佐剂性关节炎。
J Transl Med. 2016 Jun 7;14(1):162. doi: 10.1186/s12967-016-0908-7.
10
Expression levels of B7-H3 and TLT-2 in human oral squamous cell carcinoma.人口腔鳞状细胞癌中B7-H3和TLT-2的表达水平
Oncol Lett. 2015 Aug;10(2):1063-1068. doi: 10.3892/ol.2015.3274. Epub 2015 May 27.

本文引用的文献

1
The determinants of susceptibility/resistance to adjuvant arthritis in rats.大鼠对佐剂性关节炎易感性/抗性的决定因素。
Arthritis Res Ther. 2009;11(4):239. doi: 10.1186/ar2755. Epub 2009 Aug 7.
2
Pharmacometabonomic identification of a significant host-microbiome metabolic interaction affecting human drug metabolism.影响人体药物代谢的重要宿主-微生物群代谢相互作用的药物代谢组学鉴定。
Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14728-33. doi: 10.1073/pnas.0904489106. Epub 2009 Aug 10.
3
Geranylgeranylacetone, a non-toxic inducer of heat shock protein, induces cell death in fibroblast-like synoviocytes from patients with rheumatoid arthritis.香叶基香叶基丙酮是一种无毒的热休克蛋白诱导剂,可诱导类风湿关节炎患者的成纤维样滑膜细胞发生细胞死亡。
Mod Rheumatol. 2009;19(4):379-83. doi: 10.1007/s10165-009-0183-z. Epub 2009 Jun 13.
4
Heat shock protein 96 is elevated in rheumatoid arthritis and activates macrophages primarily via TLR2 signaling.热休克蛋白96在类风湿性关节炎中升高,并主要通过Toll样受体2信号通路激活巨噬细胞。
J Immunol. 2009 Apr 15;182(8):4965-73. doi: 10.4049/jimmunol.0801563.
5
IL-10 is critically involved in mycobacterial HSP70 induced suppression of proteoglycan-induced arthritis.白细胞介素-10在分枝杆菌热休克蛋白70诱导的蛋白聚糖诱导性关节炎抑制中起关键作用。
PLoS One. 2009;4(1):e4186. doi: 10.1371/journal.pone.0004186. Epub 2009 Jan 14.
6
The differential expressions of 78-kDa glucose-regulated protein of infiltrating plasma cells in peripheral joints with the histopathological variants of rheumatoid synovitis.浸润性浆细胞在类风湿关节炎滑膜组织中不同组织病理学表型的 78kDa 葡萄糖调节蛋白的差异表达。
Arthritis Res Ther. 2009 Jan 9;11(1):R4. doi: 10.1186/ar2588.
7
Tolerization with Hsp65 induces protection against adjuvant-induced arthritis by modulating the antigen-directed interferon-gamma, interleukin-17, and antibody responses.用热休克蛋白65进行耐受诱导可通过调节抗原导向的干扰素-γ、白细胞介素-17和抗体反应来诱导对佐剂诱导性关节炎的保护作用。
Arthritis Rheum. 2009 Jan;60(1):103-13. doi: 10.1002/art.24139.
8
Small molecule inhibitors of Hsp90 potently affect inflammatory disease pathways and exhibit activity in models of rheumatoid arthritis.热休克蛋白90(Hsp90)的小分子抑制剂能有效影响炎症性疾病通路,并在类风湿性关节炎模型中表现出活性。
Arthritis Rheum. 2008 Dec;58(12):3765-75. doi: 10.1002/art.24047.
9
HMOX1 promoter polymorphism modulates the relationship between disease activity and joint damage in rheumatoid arthritis.HMOX1启动子多态性调节类风湿关节炎中疾病活动与关节损伤之间的关系。
Arthritis Rheum. 2008 Nov;58(11):3388-93. doi: 10.1002/art.23970.
10
Epitope spreading to citrullinated antigens in mouse models of autoimmune arthritis and demyelination.在自身免疫性关节炎和脱髓鞘的小鼠模型中,表位扩展至瓜氨酸化抗原。
Arthritis Res Ther. 2008;10(5):R119. doi: 10.1186/ar2523. Epub 2008 Sep 30.

热休克蛋白在自身免疫性关节炎发病机制中的作用:批判性评价。

The involvement of heat-shock proteins in the pathogenesis of autoimmune arthritis: a critical appraisal.

机构信息

Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.

出版信息

Semin Arthritis Rheum. 2010 Oct;40(2):164-75. doi: 10.1016/j.semarthrit.2009.10.002. Epub 2009 Dec 6.

DOI:10.1016/j.semarthrit.2009.10.002
PMID:19969325
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3390779/
Abstract

OBJECTIVES

To review the literature on the role of heat-shock proteins (HSPs) in the pathogenesis of autoimmune arthritis in animal models and patients with rheumatoid arthritis (RA).

METHODS

The published literature in Medline (PubMed), including our published work on the cell-mediated as well as humoral immune response to various HSPs, was reviewed. Studies in the preclinical animal models of arthritis as well as RA were examined critically and the data are presented.

RESULTS

In experimental arthritis, disease induction by different arthritogenic stimuli, including an adjuvant, led to immune response to mycobacterial HSP65 (BHSP65). However, attempts to induce arthritis by a purified HSP have not met with success. There are several reports of a significant immune response to HSP65 in RA patients. However, the issue of cause and effect is difficult to address. Nevertheless, several studies in animal models and a couple of clinical trials in RA patients have shown the beneficial effect of HSPs against autoimmune arthritis.

CONCLUSIONS

There is a clear association between immune response to HSPs, particularly HSP65, and the initiation and propagation of autoimmune arthritis in experimental models. The correlation is relatively less convincing in RA patients. In both cases, the ability of HSPs to modulate arthritis offers support, albeit an indirect one, for the involvement of these antigens in the disease process.

摘要

目的

综述热休克蛋白(HSPs)在动物模型和类风湿关节炎(RA)患者自身免疫性关节炎发病机制中的作用的文献。

方法

检索 Medline(PubMed)上发表的文献,包括我们关于各种 HSP 细胞介导和体液免疫反应的已发表工作。对关节炎和 RA 的临床前动物模型研究进行了批判性检查,并提供了相关数据。

结果

在实验性关节炎中,不同关节炎诱发刺激物(包括佐剂)引起针对分枝杆菌 HSP65(BHSP65)的免疫反应。然而,用纯化 HSP 诱导关节炎的尝试并未成功。有几项报道称 RA 患者对 HSP65 有明显的免疫反应。然而,因果关系很难确定。尽管如此,一些动物模型研究和几项 RA 患者的临床试验表明 HSPs 对自身免疫性关节炎具有有益作用。

结论

在实验模型中,HSPs(尤其是 HSP65)的免疫反应与自身免疫性关节炎的起始和传播之间存在明确的关联。在 RA 患者中,相关性的说服力相对较低。在这两种情况下,HSP 调节关节炎的能力为这些抗原参与疾病过程提供了支持,尽管是间接的支持。