Dysregulation of IL-34 ligation to SDC-1 mitigates collagen-induced arthritis  

作　　者：Anja Meyer Ryan Sienes Brian Zanotti Katrien van Raemdonck Karol Palasiewicz Daniel P.Mass Michael V.Volin Shiva Shahrara 

机构地区：[1]Jesse Brown VA Medical Center,Chicago,IL,USA [2]Department of Medicine,Division of Rheumatology,The University of Illinois at Chicago,Chicago,IL,USA [3]Department of Microbiology and Immunology,Midwestern University,Downers Grove,IL,USA [4]Department of Orthopedic Surgery,The University of Illinois at Chicago,Chicago,IL,USA

出　　处：《Cellular & Molecular Immunology》2022年第9期1070-1072,共3页中国免疫学杂志（英文版）

基　　金：This work was supported in part by awards from the Department of Veteran’s Affairs MERIT Award BX002286;the Innovative Research Award from the Rheumatology Research Foundation(RRF);the National Institutes of Health NIH AI147697;the National Psoriasis Foundation(NPF);the Pfizer Investigator-Initiated Research(IIR)Program;the Chicago Biomedical Consortium(CBC)Accelerator Award.

摘　　要：IL-34 is a novel biomarker for rheumatoid arthritis(RA),as its serum levels are linked to C-reactive protein,erythrocyte sedimentation rate,rheumatoid factor(RF),IL-6 and radiographic progression[1,2].IL-34 reprograms naïve circulating M0 cells into glycolytic(CD14^(+)CD86^(+)GLUT1^(high))M34 macrophages(MΦs)by binding to its pathogenic receptor,SDC-1,which controls the activation of its coreceptor/M-CSFR[3].Glycolytic M34 MΦs are primed to differentiate into osteoclasts through SDC-1 ligation[3].

关 键 词：CD86 GLUT1 SEDIMENTATION 

分 类 号：R593.22[医药卫生—内科学]