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| 1 | Macrophages are the primary effector cells in IL-7-induced arthritis显示文摘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 macrophages.The 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 induction.Hence, 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. | 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 | 2020 | Cellular & Molecular Immunology2020，17，7： | 4 |
| 2 | Dimethyl Sulfide in the Surface Ocean and the Marine Atmosphere:A Global View显示文摘 | Andreae M O Hans Raemdonck | 1983 | Science1983，221，： | 1 |
| 3 | External cooling of warm ischemic rabbit lungs after death显示文摘 | Van Raemdonck DE Jannis NC Rega FR | 1996 | Ann Thoracic Surgery1996，62，： | 1 |
| 4 | Accuracy of exhaled nitric oxide measurements for the diagnosis of bronchiolitis obliterans syndrome after lung transplantation显示文摘 | Verleden GM Dupont LJ Van Raemdonck DE | 2004 | Transplantation2004，78，： | 1 |
| 5 | Donation after circulatory death:current status显示文摘 | Neyrinck A Van Raemdonck D Monbaliu D | 2013 | Curr Opin Anaesthesiol2013，26，3： | 1 |
| 6 | Massive lung collapse with partial resolution after several years : a case report 显示文摘 | Govaere E Van Raemdonck D Devlieger H | 2005 | BMC Pediatr2005，5，1： | 1 |
| 7 | Management of thymic tumors: a survey of current practice among members of the European Society of Thoracic Surgeons显示文摘 | RUFFINI E VAN RAEMDONCK D DETTERBECK F | 2011 | J Thorac Oneal2011，6，3： | 1 |
| 8 | Massive lungcollapse with partial resolution after several years: a case report 显示文摘 | Govaere E Raemdonck DV Devlieger H | 2005 | BMC Pdiatrics2005，5，10： | 1 |
| 9 | Dimethyl sulfur in the surface ocean and the marine atmosphere:A global view显示文摘 | Andreae M O Raemdonck H | 1983 | Science1983，221，： | 1 |
| 10 | Primary cryptoeoccal cellulitis in a lung transplant recipient 显示文摘 | Van Grieken SA Dupont LJ Van Raemdonck DE | 2007 | The Journal of Heart and Lung Transplantation2007，26，3： | 1 |
| 11 | Maintaining the silence:reflections on long-term RNAi显示文摘 | Raemdonck K Vandenbroucke R E Demeester J | 2008 | Drug Discovery Today2008，13，2122： | 1 |
| 12 | Autocrine CCL2,CXC14,CX-CI^ and CXCLlO signal in retinal endothelial cells and are enhanced in diabetic retinopathy显示文摘 | Nawaz MI Van Raemdonck K Mohammad G Kangave D Van Damme J Abu El-Asrar AM | 2013 | Eocp Eye Res2013，109，： | 1 |
| 13 | Lung transplantation: a 15-year single-center experience 显示文摘 | Verleden GM Dupont LJ Van Raemdonck DE | 2007 | Clin Transplant2007，，： | 1 |
| 14 | Pulmonary sequestration:a comparison between pediatric and adult patients显示文摘 | Van Raemdonck D De Boeck K Devlieger H | | 0，，： | 1 |
| 15 | Lobar lung transplantation from deceased donors: A systematic review显示文摘AIM To systematically review reports on deceased-donor-lobar lung transplantation(dd LLTx) and uniformly describe sizematching using the donor-to-recipient predicted-total lung-capacity(pT LC) ratio. METHODS We set out to systematically review reports on ddL LTx and uniformly describe size matching using the donorto-recipient pT LC ratio and to summarize reported oneyear survival data of ddL LTx and conventional-LTx. We searched in Pub Med, CINAHL via EBSCO, Cochrane Database of Systematic Reviews via Wiley(CDSR),Database of Abstracts of Reviews of Effects via Wiley(DARE), Cochrane Central Register of Controlled Trials via Wiley(CENTRAL), Scopus(which includes EMBASE abstracts), and Web of Science for original reports on ddL LTx. RESULTS Nine observational cohort studies reporting on 301 ddL LTx met our inclusion criteria for systematic review of size matching, and eight for describing one-year-survival. The dd LLTx-group was often characterized by high acuity;however there was heterogeneity in transplant indications and pre-operative characteristics between studies. Data to calculate the pT LC ratio was available for 242 ddL LTx(80%). The mean pT LCratio before lobar resection was1.25 ± 0.3 and the transplanted pT LCratio after lobar resection was 0.76 ± 0.2. One-year survival in the ddL LTxgroup ranged from 50%-100%, compared to 72%-88%in the conventional-LTx group. In the largest study ddL LTx(n = 138) was associated with a lower one-year-survival compared to conventional-LTx(n = 539)(65.1% vs84.1%, P < 0.001). CONCLUSION Further investigations of optimal donor-to-recipient size matching parameters for ddL LTx could improve outcomes of this important surgical option. | Michael Eberlein Robert M Reed Mayy Chahla Servet Bolukbas Amy Blevins Dirk Van Raemdonck Alessia Stanzi Ilhan Inci Silvana Marasco Norihisa Shigemura Clemens Aigner Tobias Deuse | 2017 | World Journal of Transplantation2017，7，1： | 1 |
| 16 | Extemal cooling of warm ischemic rabbit lungs after death显示文摘 | Van Raemdonck DE Jannis NC Rega FR | 1996 | Ann Thoracic Surgery1996，62，： | 1 |
| 17 | Polysaccharide-based nucleic acid nanoformulations显示文摘 | Raemdonck K Martens T F Braeckmans K | 2013 | Advanced Drug Delivery Reviews2013，65，9： | 1 |
| 18 | Enhanced Fibroblast Contraction of 3D Collagen Lattices and Integrin Expression by TGF-β1 and -β3: Mechanoregulatory Growth Factors?显示文摘 | Robert A. Brown Kamaljit K. Sethi Ivo Gwanmesia David Raemdonck Mark Eastwood Vivek Mudera | 2002 | Experimental Cell Research2002，，2： | 1 |
| 19 | Dimethylsulfide in the surface ocean and the marine atmophere:A global view显示文摘 | M O and Raemdonck H | 1983 | Science1983，221，： | 1 |
| 20 | IRAK4 inhibition: a promising strategy for treating RA joint inflammation and bone erosion显示文摘Flares of joint inflammation and resistance to currently available biologic therapeutics in rheumatoid arthritis(RA)patients could reflect activation of innate immune mechanisms.Herein,we show that a TLR7 GU-rich endogenous ligand,miR-Let7b,potentiates synovitis by amplifying RA monocyte and fibroblast(FLS)trafficking.miR-Let7b ligation to TLR7 in macrophages(MΦs)and FLSs expanded the synovial inflammatory response.Moreover,secretion of M1 monokines triggered by miR-Let7b enhanced Th1/Th17 cell differentiation.We 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 polarization.IRAK4i therapy also disrupted RA osteoclastogenesis,which was amplified by miR-Let7b ligation to joint myeloid TLR7.Hence,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 arthritis.We 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 differentiation.Unexpectedly,these biologic therapies were unable to alleviate miR-Let7b-induced arthritis.The 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 lymphokines.In conclusion,IRAK4i therapy may provide a promising strategy for RA therapy by disconnecting critical links between inflammatory joint cells. | 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 | 2021 | Cellular & Molecular Immunology2021，18，9： | 1 |
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