• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

Toll 样受体和 NOD 样受体在风湿性疾病中的作用。

Toll-like receptors and NOD-like receptors in rheumatic diseases.

机构信息

OPSONA Therapeutics Ltd, Institute of Molecular Medicine, Trinity Centre for Health Sciences, St James' Hospital, Dublin 8, Ireland.

出版信息

Arthritis Res Ther. 2009;11(5):243. doi: 10.1186/ar2729. Epub 2009 Oct 14.

DOI:10.1186/ar2729
PMID:19835640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2787278/
Abstract

The past 10 years have seen the description of families of receptors that drive proinflammatory cytokine production in infection and tissue injury. Two major classes have been examined in the context of inflammatory joint disease--the Toll-like receptors (TLRs) and NOD-like receptors (NLRs). TLRs such as TLR2 and TLR4 are being implicated in the pathology of rheumatoid arthritis, ankylosing spondylitis, lyme arthritis and osteoarthritis. Nalp3 has been identified as a key NLR for IL-1beta production and has been shown to have a particular role in gout. These findings present new therapeutic opportunities, possibly allowing for the replacement of biologics with small molecule inhibitors.

摘要

过去十年见证了能够驱动感染和组织损伤中促炎细胞因子产生的受体家族的描述。在炎症性关节疾病的背景下，已经研究了两大类-- Toll 样受体 (TLR) 和 NOD 样受体 (NLR)。TLR 如 TLR2 和 TLR4 被认为与类风湿关节炎、强直性脊柱炎、莱姆关节炎和骨关节炎的病理学有关。NALP3 已被确定为产生 IL-1β的关键 NLR，并已显示在痛风中具有特殊作用。这些发现提出了新的治疗机会，可能允许用小分子抑制剂替代生物制剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4a0/2787278/69ee1029e3d7/ar2729-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4a0/2787278/c809e021c062/ar2729-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4a0/2787278/69ee1029e3d7/ar2729-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4a0/2787278/c809e021c062/ar2729-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4a0/2787278/69ee1029e3d7/ar2729-2.jpg

相似文献

1
Toll-like receptors and NOD-like receptors in rheumatic diseases. Toll 样受体和 NOD 样受体在风湿性疾病中的作用。
Arthritis Res Ther. 2009;11(5):243. doi: 10.1186/ar2729. Epub 2009 Oct 14.
2
Understanding and modulating the Toll like Receptors (TLRs) and NOD like Receptors (NLRs) cross talk in type 2 diabetes.了解并调节2型糖尿病中Toll样受体（TLRs）和NOD样受体（NLRs）的相互作用。
Curr Diabetes Rev. 2014 May;10(3):190-200. doi: 10.2174/1573399810666140515112609.
3
Inflammasomes in inflammatory disorders: the role of TLRs and their interactions with NLRs.炎症性疾病中的炎性小体：Toll样受体的作用及其与核苷酸结合寡聚化结构域样受体的相互作用
Semin Immunopathol. 2007 Sep;29(3):239-48. doi: 10.1007/s00281-007-0081-4. Epub 2007 Sep 6.
4
Toll-like receptors (TLRs) and Nod-like receptors (NLRs) in inflammatory disorders.炎症性疾病中的Toll样受体（TLRs）和核苷酸结合寡聚化结构域样受体（NLRs）
Semin Immunol. 2009 Aug;21(4):242-53. doi: 10.1016/j.smim.2009.06.005.
5
The inflammasomes: guardians of the body.炎性小体：身体的守护者。
Annu Rev Immunol. 2009;27:229-65. doi: 10.1146/annurev.immunol.021908.132715.
6
NOD-Like Receptors in Infection, Immunity, and Diseases.感染、免疫和疾病中的NOD样受体
Yonsei Med J. 2016 Jan;57(1):5-14. doi: 10.3349/ymj.2016.57.1.5.
7
Toll-like receptors and chronic inflammation in rheumatic diseases: new developments. Toll 样受体与风湿性疾病中的慢性炎症：新进展。
Nat Rev Rheumatol. 2016 Jun;12(6):344-57. doi: 10.1038/nrrheum.2016.61. Epub 2016 May 12.
8
Toll-like receptors and NOD-like receptors: domain architecture and cellular signalling.Toll样受体和NOD样受体：结构域架构与细胞信号传导
Adv Exp Med Biol. 2009;653:48-57. doi: 10.1007/978-1-4419-0901-5_4.
9
[The interaction between Toll-like receptors and nucleotide-binding oligomerization domain proteins in defensive responses].[Toll样受体与核苷酸结合寡聚化结构域蛋白在防御反应中的相互作用]
Sheng Li Ke Xue Jin Zhan. 2006 Jul;37(3):233-5.
10
Potential link between the immune system and metabolism of nucleic acids.免疫系统与核酸代谢之间的潜在联系。
Curr Opin Immunol. 2008 Oct;20(5):524-9. doi: 10.1016/j.coi.2008.07.002. Epub 2008 Aug 6.

引用本文的文献

1
Discovery of ETI41 and ETI60: novel selective endosomal Toll-like receptor inhibitors for the treatment of autoimmune diseases.ETI41和ETI60的发现：用于治疗自身免疫性疾病的新型选择性内体Toll样受体抑制剂。
Exp Mol Med. 2025 Sep 1. doi: 10.1038/s12276-025-01526-w.
2
Modulation of IRAK4 as a Therapeutic Strategy Against Monosodium Urate- and Xanthine-Induced Inflammation in Macrophages and HepG2 Cells.调节白细胞介素-1受体相关激酶4作为对抗尿酸钠和黄嘌呤诱导的巨噬细胞和肝癌细胞系炎症的治疗策略
Res Sq. 2025 Jul 16:rs.3.rs-6908346. doi: 10.21203/rs.3.rs-6908346/v1.
3
Risk of Gout Among Patients With Tuberculosis: A Nationwide Cohort Study in South Korea.

本文引用的文献

1
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.
2
Advances in understanding calcium-containing crystal disease.含钙晶体疾病认识的进展
Curr Opin Rheumatol. 2009 Mar;21(2):150-7. doi: 10.1097/BOR.0b013e3283257ba9.
3
The inflammasomes: guardians of the body.炎性小体：身体的守护者。
肺结核患者中痛风的风险：韩国一项全国性队列研究
Int J Rheum Dis. 2025 Mar;28(3):e70197. doi: 10.1111/1756-185X.70197.
4
Anti-inflammatory Properties of Tongfeng Li'an Granules in an Acute Gouty Arthritis Rat Model.痛风立安颗粒在急性痛风性关节炎大鼠模型中的抗炎特性
ACS Omega. 2024 Jul 31;9(32):34303-34313. doi: 10.1021/acsomega.4c00056. eCollection 2024 Aug 13.
5
Recent progress in understanding mitokines as diagnostic and therapeutic targets in hepatocellular carcinoma.将线粒体因子作为肝细胞癌诊断和治疗靶点的最新进展。
World J Clin Cases. 2023 Aug 16;11(23):5416-5429. doi: 10.12998/wjcc.v11.i23.5416.
6
Psoriatic arthritis: review of potential biomarkers predicting response to TNF inhibitors.银屑病关节炎：预测 TNF 抑制剂治疗反应的潜在生物标志物综述。
Inflammopharmacology. 2023 Feb;31(1):77-87. doi: 10.1007/s10787-022-01092-x. Epub 2022 Dec 12.
7
Association of TLR 9 gene polymorphisms with remission in patients with rheumatoid arthritis receiving TNF-α inhibitors and development of machine learning models.TLR9 基因多态性与接受 TNF-α 抑制剂治疗的类风湿关节炎患者缓解和机器学习模型发展的关联。
Sci Rep. 2021 Oct 11;11(1):20169. doi: 10.1038/s41598-021-99625-x.
8
TLR4 Antagonism Reduces Movement-Induced Nociception and ATF-3 Expression in Experimental Osteoarthritis.Toll样受体4拮抗剂可减轻实验性骨关节炎中运动诱导的伤害感受及活化转录因子3表达。
J Pain Res. 2021 Aug 24;14:2615-2627. doi: 10.2147/JPR.S317877. eCollection 2021.
9
The N-Formyl Peptide Receptors and Rheumatoid Arthritis: A Dangerous Liaison or Confusing Relationship?N-甲酰肽受体与类风湿关节炎：危险的联姻还是混乱的关系？
Front Immunol. 2021 Jun 18;12:685214. doi: 10.3389/fimmu.2021.685214. eCollection 2021.
10
The Damage-Associated Molecular Patterns (DAMPs) as Potential Targets to Treat Osteoarthritis: Perspectives From a Review of the Literature.损伤相关分子模式（DAMPs）作为治疗骨关节炎的潜在靶点：文献综述视角
Front Med (Lausanne). 2021 Jan 18;7:607186. doi: 10.3389/fmed.2020.607186. eCollection 2020.
Annu Rev Immunol. 2009;27:229-65. doi: 10.1146/annurev.immunol.021908.132715.
4
Expression, regulation, and signaling of the pattern-recognition receptor nucleotide-binding oligomerization domain 2 in rheumatoid arthritis synovial fibroblasts.类风湿关节炎滑膜成纤维细胞中模式识别受体核苷酸结合寡聚化结构域2的表达、调控及信号传导
Arthritis Rheum. 2009 Feb;60(2):355-63. doi: 10.1002/art.24226.
5
The interleukin-1 receptor/Toll-like receptor superfamily: 10 years of progress.白细胞介素-1受体/Toll样受体超家族：十年进展
Immunol Rev. 2008 Dec;226:10-8. doi: 10.1111/j.1600-065X.2008.00701.x.
6
An orthogonal proteomic-genomic screen identifies AIM2 as a cytoplasmic DNA sensor for the inflammasome.一项正交蛋白质组学-基因组学筛选确定AIM2为炎性小体的细胞质DNA传感器。
Nat Immunol. 2009 Mar;10(3):266-72. doi: 10.1038/ni.1702. Epub 2009 Jan 21.
7
AIM2 activates the inflammasome and cell death in response to cytoplasmic DNA.AIM2响应细胞质DNA激活炎性小体和细胞死亡。
Nature. 2009 Mar 26;458(7237):509-13. doi: 10.1038/nature07710. Epub 2009 Jan 21.
8
AIM2 recognizes cytosolic dsDNA and forms a caspase-1-activating inflammasome with ASC.AIM2可识别胞质双链DNA，并与ASC形成激活半胱天冬酶-1的炎性小体。
Nature. 2009 Mar 26;458(7237):514-8. doi: 10.1038/nature07725. Epub 2009 Jan 21.
9
Soluble and particulate Co-Cr-Mo alloy implant metals activate the inflammasome danger signaling pathway in human macrophages: a novel mechanism for implant debris reactivity.可溶性和颗粒性钴铬钼合金植入金属激活人类巨噬细胞中的炎性小体危险信号通路：植入物碎片反应性的一种新机制。
J Orthop Res. 2009 Jul;27(7):847-54. doi: 10.1002/jor.20826.
10
Induction of inflammatory and immune responses by HMGB1-nucleosome complexes: implications for the pathogenesis of SLE.HMGB1-核小体复合物诱导炎症和免疫反应：对系统性红斑狼疮发病机制的影响
J Exp Med. 2008 Dec 22;205(13):3007-18. doi: 10.1084/jem.20081165. Epub 2008 Dec 8.