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

Cellular & Molecular Immunology 2022年第9期19卷 1070-1072页

作者： Anja Meyer Ryan Sienes Brian Zanotti Katrien van Raemdonck karol palasiewicz Daniel P.Mass Michael V.Volin Shiva Shahrara Jesse Brown VA Medical Center ChicagoILUSA Department of Medicine Division of RheumatologyThe University of Illinois at ChicagoChicagoILUSA Department of Microbiology and Immunology Midwestern UniversityDowners GroveILUSA Department of Orthopedic Surgery The University of Illinois at ChicagoChicagoILUSA

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

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

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Cellular & Molecular Immunology 2021年第9期18卷 2199-2210页

作者： Sadiq Umar karol palasiewicz Katrien Van Raemdonck Michael V.Volin Bianca Romay MAsif Amin Ryan K.Zomorrodi Shiva Arami Mark Gonzalez Vikram Rao Brian Zanotti David A.Fox Nadera Sweiss Shiva Shahrara Jesse Brown VA Medical Center ChicagoIL60612USA Department of Medicine Division of RheumatologyUniversity of Illinois at ChicagoChicagoIL60612USA Department of Microbiology and Immunology Midwestern UniversityDowners GroveIL60515USA Division of Rheumatology and Clinical Autoimmunity Center of Excellence University of MichiganAnn ArborMI481096USA Department of Orthopedic Surgery University of Illinois at ChicagoChicagoIL60612USA Pfizer Research CambridgeMA02139USA

Flares of joint inflammation and resistance to currently available biologic therapeutics in rheumatoid arthritis(RA)patients could reflect activation of innate immune ***,we show that a TLR7 GU-rich endogenous ligand,miR-Let7b,potentiates synovitis by amplifying RA monocyte and fibroblast(FLS)***-Let7b ligation to TLR7 in macrophages(MΦs)and FLSs expanded the synovial inflammatory ***,secretion of M1 monokines triggered by miR-Let7b enhanced Th1/Th17 cell *** showed that IRAK4 inhibitor(i)therapy attenuated RA disease activity by blocking TLR7-induced M1 MΦor FLS activation,as well as monokine-modulated Th1/Th17 cell ***4i therapy also disrupted RA osteoclastogenesis,which was amplified by miR-Let7b ligation to joint myeloid ***,the effectiveness of IRAK4i was compared with that of a TNF inhibitor(i)or anti-IL-6R treatment in collagen-induced arthritis(CIA)and miR-Let7b-mediated *** found that TNF or IL-6R blocking therapies mitigated CIA by reducing the infiltration of joint F480+iNOS+MΦs,the expression of certain monokines,and Th1 cell ***,these biologic therapies were unable to alleviate miR-Let7b-induced *** superior efficacy of IRAK4i over anti-TNF or anti-IL-6R therapy in miR-Let7b-induced arthritis or CIA was due to the ability of IRAK4i therapy to restrain the migration of joint F480+iNOS+MΦs,vimentin+fibroblasts,and CD3+T cells,in addition to negating the expression of a wide range of monokines,including IL-12,MIP2,and IRF5 and Th1/Th17 *** conclusion,IRAK4i therapy may provide a promising strategy for RA therapy by disconnecting critical links between inflammatory joint cells.

关键词： TLR7 MΦs RA FLSs osteoclasts T cells IRAK4

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

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Cellular & Molecular Immunology 2020年第7期17卷 728-740页

作者： Seung-jae Kim Huan J.Chang Michael VVolin 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 Division of Rheumatology Jesse Brown VAMedical CenterChicagoIL 60612USA Department of Medicine Division of RheumatologyUniversity of Illinois at ChicagoChicagoIL 60612USA Department of Microbiology and Immunology Chicago College of Osteopathic MedicineMidwestern UniversityDowners GroveIL 60515USA Pulmonary Critical Care and Sleep MedicineOhio State University Wexner Medical CenterDavis Heart and Lung Research InstituteColumbusOH 43210USA Division of Allergy Clinical Immunology and RheumatologyThe University of Kansas Medical CenterKansas CityKS 66160USA Division of Rheumatology and Clinical Autoimmunity Center of Excellence University of MichiganAnn ArborMI 481096USA

Synovial macrophages are crucial in the development of joint inflammation and bone damage;however, the pathways that controlmacrophage remodeling in inflammatory M1 cells or bone-eroding osteoclasts are not fully understood. We determined thatelevated IL-7R/CD127 expression is the hallmark of rheumatoid arthritis (RA) M1 macrophages and that these cells are highlyresponsive to interleukin-7 (IL-7)-driven osteoclastogenesis. We established that lipopolysaccharide (LPS), interferon-γ (IFNγ), andtumor necrosis factor-α (TNFα), the classic M1 macrophage mediators, enhance IL-7R expression in RA and murine *** local expression of IL-7 provokes arthritis, predominantly through escalating the number of F480^(+)iNOS^(+) cells rather than CD3^(+)T cells. Ectopic LPS injection stabilizes IL-7-induced arthritis by increasing myeloid IL-7R expression, in part via IFNγ ***, in RAG−/− mice, IL-7-mediated arthritis is suppressed because of the reduction in myeloid IL-7R expression due to the lackof IFNγ. Moreover, the amelioration of IL-7-induced arthritis by anti-TNF therapy is due to a decrease in the number of cells in theunique F480^(+)iNOS^(+)IL-7R^(+)CCL5^(+) subset, with no impact on the F480^(+)Arginase^(+) cell or CD3^(+) T cell frequency. Consistent with thepreclinical findings, the findings of a phase 4 study performed with RA patients following 6 months of anti-TNF therapy revealedthat IL-7R expression was reduced without affecting the levels of IL-7. This study shifts the paradigm by discovering that IL-7-induced arthritis is dependent on F480^(+)iNOS^(+)IL-7R^(+)CCL5^(+) cell function, which activates TH-1 cells to amplify myeloid IL-7Rexpression and disease severity.

关键词： myeloid elevated inflammation

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