Nadera Sweiss相关文献与解析，生知库 | 链接生命科学的每一步

Sadiq Umar, Karol Palasiewicz, Katrien Van Raemdonck, Michael V Volin, Bianca Romay, M Asif Amin, Ryan K Zomorrodi, Shiva Arami, Mark Gonzalez, Vikram Rao, Brian Zanotti, David A Fox, Nadera Sweiss, Shiva Shahrara

免疫

关节炎

Immunology/Inflammation

发表日期：2021

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Interleukin-34 Reprograms Glycolytic and Osteoclastic Rheumatoid Arthritis Macrophages via Syndecan 1 and Macrophage Colony-Stimulating Factor Receptor

白细胞介素-34 通过 Syndecan 1 和巨噬细胞集落刺激因子受体重新编程糖酵解和破骨性类风湿关节炎巨噬细胞

期刊:Arthritis & Rheumatology

影响因子:11.4

doi:10.1002/art.41792

Katrien Van Raemdonck, Sadiq Umar, Karol Palasiewicz, Michael V Volin, Hatem A Elshabrawy, Bianca Romay, Chandana Tetali, Azam Ahmed, M Asif Amin, Ryan K Zomorrodi, Nadera Sweiss, Shiva Shahrara

Metabolic regulation of RA macrophages is distinct from RA fibroblasts and blockade of glycolysis alleviates inflammatory phenotype in both cell types

RA 巨噬细胞的代谢调节与 RA 成纤维细胞不同，阻断糖酵解可减轻两种细胞类型的炎症表型

期刊:Cellular and Molecular Life Sciences

影响因子:6.2

doi:10.1007/s00018-021-03978-5

Sadiq Umar, Karol Palasiewicz, Michael V Volin, Bianca Romay, Rani Rahat, Chandana Tetali, Shiva Arami, Monica Guma, Christian Ascoli, Nadera Sweiss, Ryan K Zomorrodi, Luke A J O'Neill, Shiva Shahrara

IRAK4 inhibitor mitigates joint inflammation by rebalancing metabolism malfunction in RA macrophages and fibroblasts

IRAK4抑制剂通过重新平衡RA巨噬细胞和成纤维细胞中的代谢功能障碍来减轻关节炎症。

期刊:Life Sciences

影响因子:5.2

doi:10.1016/j.lfs.2021.120114

Sadiq Umar ,Karol Palasiewicz ,Michael V Volin ,Brian Zanotti ,Mina Al-Awqati ,Nadera Sweiss ,Shiva Shahrara

CCL25 and CCR9 is a unique pathway that potentiates pannus formation by remodeling RA macrophages into mature osteoclasts

CCL25 和 CCR9 是一种独特的途径，它通过将 RA 巨噬细胞重塑为成熟破骨细胞来增强血管翳的形成

期刊:European Journal of Immunology

影响因子:4.5

doi:10.1002/eji.202048681

Sadiq Umar, Karol Palasiewicz, Katrien Van Raemdonck, Michael V Volin, Bianca Romay, Imran Ahmad, Chandana Tetali, Nadera Sweiss, M Asif Amin, Ryan K Zomorrodi, Shiva Shahrara

TLR7 endogenous ligands remodel glycolytic macrophages and trigger skin-to-joint crosstalk in psoriatic arthritis

TLR7 内源性配体重塑糖酵解巨噬细胞并引发银屑病关节炎中的皮肤与关节串扰

期刊:European Journal of Immunology

影响因子:4.5

doi:10.1002/eji.202048690

Katrien Van Raemdonck, Sadiq Umar, Karol Palasiewicz, Bianca Romay, Suncica Volkov, Shiva Arami, Nadera Sweiss, Shiva Shahrara

Macrophages are the primary effector cells in IL-7-induced arthritis

巨噬细胞是IL-7诱导的关节炎中的主要效应细胞。

期刊:Cellular & Molecular Immunology

影响因子:21.8

doi:10.1038/s41423-019-0235-z

Seung-Jae Kim ，Huan J Chang ，Michael V Volin ，Sadiq Umar ，Katrien Van Raemdonck ，Aimee Chevalier ，Karol Palasiewicz ，John W Christman ，Suncica Volkov ，Shiva Arami ，Mehrdad Maz ，Anjali Mehta ，Ryan K Zomorrodi ，David A Fox ，Nadera Sweiss ，Shiva Shahrara

CCL21/CCR7 signaling in macrophages promotes joint inflammation and Th17-mediated osteoclast formation in rheumatoid arthritis

巨噬细胞中的 CCL21/CCR7 信号促进类风湿关节炎中的关节炎症和 Th17 介导的破骨细胞形成

期刊:Cellular and Molecular Life Sciences

影响因子:6.2

doi:10.1007/s00018-019-03235-w

Katrien Van Raemdonck, Sadiq Umar, Karol Palasiewicz, Suncica Volkov, Michael V Volin, Shiva Arami, Huan J Chang, Brian Zanotti, Nadera Sweiss, Shiva Shahrara

Immunology/Inflammation

发表日期：2020

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Identification of a Novel Toll-like Receptor 7 Endogenous Ligand in Rheumatoid Arthritis Synovial Fluid That Can Provoke Arthritic Joint Inflammation

鉴定类风湿关节炎滑液中可引发关节炎性关节炎的新型 Toll 样受体 7 内源性配体

期刊:Arthritis & Rheumatology

影响因子:11.4

doi:10.1002/art.39544

Seung-Jae Kim, Zhenlong Chen, Abdul B Essani, Hatem A Elshabrawy, Michael V Volin, Suncica Volkov, William Swedler, Shiva Arami, Nadera Sweiss, Shiva Shahrara

Ligation of TLR5 promotes myeloid cell infiltration and differentiation into mature osteoclasts in rheumatoid arthritis and experimental arthritis

在类风湿性关节炎和实验性关节炎中，TLR5 的连接促进髓系细胞浸润并分化为成熟破骨细胞

期刊:Journal of Immunology

影响因子:3.6

doi:10.4049/jimmunol.1302998

Seung-Jae Kim, Zhenlong Chen, Nathan D Chamberlain, Abdul B Essani, Michael V Volin, M Asif Amin, Suncica Volkov, Ellen M Gravallese, Shiva Arami, William Swedler, Nancy E Lane, Anjali Mehta, Nadera Sweiss, Shiva Shahrara

IRAK4 inhibition: a promising strategy for treating RA joint inflammation and bone erosion

IRAK4 抑制：治疗 RA 关节炎症和骨质侵蚀的一种有前景的策略

Interleukin-34 Reprograms Glycolytic and Osteoclastic Rheumatoid Arthritis Macrophages via Syndecan 1 and Macrophage Colony-Stimulating Factor Receptor

白细胞介素-34 通过 Syndecan 1 和巨噬细胞集落刺激因子受体重新编程糖酵解和破骨性类风湿关节炎巨噬细胞

Metabolic regulation of RA macrophages is distinct from RA fibroblasts and blockade of glycolysis alleviates inflammatory phenotype in both cell types

RA 巨噬细胞的代谢调节与 RA 成纤维细胞不同，阻断糖酵解可减轻两种细胞类型的炎症表型

IRAK4 inhibitor mitigates joint inflammation by rebalancing metabolism malfunction in RA macrophages and fibroblasts

IRAK4抑制剂通过重新平衡RA巨噬细胞和成纤维细胞中的代谢功能障碍来减轻关节炎症。

CCL25 and CCR9 is a unique pathway that potentiates pannus formation by remodeling RA macrophages into mature osteoclasts

CCL25 和 CCR9 是一种独特的途径，它通过将 RA 巨噬细胞重塑为成熟破骨细胞来增强血管翳的形成

TLR7 endogenous ligands remodel glycolytic macrophages and trigger skin-to-joint crosstalk in psoriatic arthritis

TLR7 内源性配体重塑糖酵解巨噬细胞并引发银屑病关节炎中的皮肤与关节串扰

Macrophages are the primary effector cells in IL-7-induced arthritis

巨噬细胞是IL-7诱导的关节炎中的主要效应细胞。

CCL21/CCR7 signaling in macrophages promotes joint inflammation and Th17-mediated osteoclast formation in rheumatoid arthritis

巨噬细胞中的 CCL21/CCR7 信号促进类风湿关节炎中的关节炎症和 Th17 介导的破骨细胞形成

Identification of a Novel Toll-like Receptor 7 Endogenous Ligand in Rheumatoid Arthritis Synovial Fluid That Can Provoke Arthritic Joint Inflammation

鉴定类风湿关节炎滑液中可引发关节炎性关节炎的新型 Toll 样受体 7 内源性配体

Ligation of TLR5 promotes myeloid cell infiltration and differentiation into mature osteoclasts in rheumatoid arthritis and experimental arthritis

在类风湿性关节炎和实验性关节炎中，TLR5 的连接促进髓系细胞浸润并分化为成熟破骨细胞