Pathogenic role and clinical significance of neutrophils and neutrophil extracellular traps in idiopathic inflammatory myopathies.

Autoimmune diseases Idiopathic inflammatory myopathies Low-density granulocytes Neutrophil extracellular traps

Journal

Clinical and experimental medicine
ISSN: 1591-9528
Titre abrégé: Clin Exp Med
Pays: Italy
ID NLM: 100973405

Informations de publication

Date de publication:
30 May 2024
Historique:
received: 08 04 2024
accepted: 21 05 2024
medline: 30 5 2024
pubmed: 30 5 2024
entrez: 30 5 2024
Statut: epublish

Résumé

Idiopathic inflammatory myopathies (IIM) are a heterogeneous group of chronic autoimmune diseases characterized by muscle damage and extramuscular symptoms, including specific skin rash, arthritis, interstitial lung disease, and cardiac involvement. While the etiology and pathogenesis of IIM are not yet fully understood, emerging evidence suggests that neutrophils and neutrophil extracellular traps (NETs) have a role in the pathogenesis. Recent research has identified increased levels of circulating and tissue neutrophils as well as NETs in patients with IIM; these contribute to the activation of the type I and type II interferons pathway. During active IIM disease, myositis-specific antibodies are associated with the formation and incomplete degradation of NETs, leading to damage in the lungs, muscles, and blood vessels of patients. This review focuses on the pathogenic role and clinical significance of neutrophils and NETs in IIM, and it includes a discussion of potential targeted treatment strategies.

Identifiants

pubmed: 38814339
doi: 10.1007/s10238-024-01384-2
pii: 10.1007/s10238-024-01384-2
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

115

Subventions

Organisme : Sichuan Province Science and Technology Support Program
ID : 2021JDRC0045 and 2021YFS0164
Organisme : Sichuan Province Science and Technology Support Program
ID : 2021JDRC0045 and 2021YFS0164
Organisme : Sichuan Province Science and Technology Support Program
ID : 2021JDRC0045 and 2021YFS0164
Organisme : Sichuan Province Science and Technology Support Program
ID : 2021JDRC0045 and 2021YFS0164
Organisme : Sichuan Province Science and Technology Support Program
ID : 2021JDRC0045 and 2021YFS0164
Organisme : Sichuan Province Science and Technology Support Program
ID : 2021JDRC0045 and 2021YFS0164

Informations de copyright

© 2024. The Author(s).

Références

Lundberg IE, et al. Idiopathic inflammatory myopathies. Nat Rev Dis Primers. 2021;7(1):86.
pubmed: 34857798 doi: 10.1038/s41572-021-00321-x
Lundberg IE, de Visser M, Werth VP. Classification of myositis. Nat Rev Rheumatol. 2018;14(5):269–78.
pubmed: 29651121 doi: 10.1038/nrrheum.2018.41
Chrysanthopoulou A, et al. Neutrophil extracellular traps promote differentiation and function of fibroblasts. J Pathol. 2014;233(3):294–307.
pubmed: 24740698 doi: 10.1002/path.4359
Miller FW, et al. Risk factors and disease mechanisms in myositis. Nat Rev Rheumatol. 2018;14(5):255–68.
pubmed: 29674613 pmcid: 6745704 doi: 10.1038/nrrheum.2018.48
Villanueva E, et al. Netting neutrophils induce endothelial damage, infiltrate tissues, and expose immunostimulatory molecules in systemic lupus erythematosus. J Immunol. 2011;187(1):538–52.
pubmed: 21613614 doi: 10.4049/jimmunol.1100450
Khandpur R, et al. NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis. Sci Transl Med. 2013;5(178):178ra40.
pubmed: 23536012 pmcid: 3727661 doi: 10.1126/scitranslmed.3005580
Grayson PC, et al. Neutrophil-related gene expression and low-density granulocytes associated with disease activity and response to treatment in antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Rheumatol. 2015;67(7):1922–32.
pubmed: 25891759 pmcid: 4485551 doi: 10.1002/art.39153
Ma W, et al. The role of neutrophil extracellular traps and proinflammatory damage-associated molecular patterns in idiopathic inflammatory myopathies. Clin Exp Immunol. 2023;213(2):202–8.
pubmed: 37289984 doi: 10.1093/cei/uxad059
Torres-Ruiz J, et al. Low-density granulocytes and neutrophil extracellular traps as biomarkers of disease activity in adult inflammatory myopathies. J Clin Rheumatol. 2022;28(2):e480–7.
pubmed: 34643846 doi: 10.1097/RHU.0000000000001772
Grayson PC, Kaplan MJ. At the bench: neutrophil extracellular traps (NETs) highlight novel aspects of innate immune system involvement in autoimmune diseases. J Leukoc Biol. 2016;99(2):253–64.
pubmed: 26432901 doi: 10.1189/jlb.5BT0615-247R
Zhang S, et al. Enhanced formation and impaired degradation of neutrophil extracellular traps in dermatomyositis and polymyositis: a potential contributor to interstitial lung disease complications. Clin Exp Immunol. 2014;177(1):134–41.
pubmed: 24611519 pmcid: 4089162 doi: 10.1111/cei.12319
Dalakas MC, Sivakumar K. The immunopathologic and inflammatory differences between dermatomyositis, polymyositis and sporadic inclusion body myositis. Curr Opin Neurol. 1996;9(3):235–9.
pubmed: 8839618 doi: 10.1097/00019052-199606000-00015
Gao S, et al. Using multi-omics methods to understand dermatomyositis/polymyositis. Autoimmun Rev. 2017;16(10):1044–8.
pubmed: 28778709 doi: 10.1016/j.autrev.2017.07.021
De Paepe B, Creus KK, De Bleecker JL. Role of cytokines and chemokines in idiopathic inflammatory myopathies. Curr Opin Rheumatol. 2009;21(6):610–6.
pubmed: 19726994 doi: 10.1097/BOR.0b013e3283317b31
Peake JM, et al. Muscle damage and inflammation during recovery from exercise. J Appl Physiol. 2017;122(3):559–70.
pubmed: 28035017 doi: 10.1152/japplphysiol.00971.2016
Robinson DCL, Dilworth FJ. Epigenetic regulation of adult myogenesis. Curr Top Dev Biol. 2018;126:235–84.
pubmed: 29305001 doi: 10.1016/bs.ctdb.2017.08.002
Filep JG. Targeting neutrophils for promoting the resolution of inflammation. Front Immunol. 2022;13:866747.
pubmed: 35371088 pmcid: 8966391 doi: 10.3389/fimmu.2022.866747
Moon SJ, et al. Molecular signature of neutrophil extracellular trap mediating disease module in idiopathic inflammatory myopathy. J Autoimmun. 2023;138:103063.
pubmed: 37220716 doi: 10.1016/j.jaut.2023.103063
Tambralli A, Gockman K, Knight JS. NETs in APS: current knowledge and future perspectives. Curr Rheumatol Rep. 2020;22(10):67.
pubmed: 32845378 doi: 10.1007/s11926-020-00936-1
Thieblemont N, et al. Human neutrophils in auto-immunity. Semin Immunol. 2016;28(2):159–73.
pubmed: 27036091 doi: 10.1016/j.smim.2016.03.004
Brinkmann V, et al. Neutrophil extracellular traps kill bacteria. Science. 2004;303(5663):1532–5.
pubmed: 15001782 doi: 10.1126/science.1092385
Brinkmann V. Neutrophil extracellular traps in the second decade. J Innate Immun. 2018;10(5–6):414–21.
pubmed: 29909412 pmcid: 6784051 doi: 10.1159/000489829
Boeltz S, et al. To NET or not to NET:current opinions and state of the science regarding the formation of neutrophil extracellular traps. Cell Death Differ. 2019;26(3):395–408.
pubmed: 30622307 pmcid: 6370810 doi: 10.1038/s41418-018-0261-x
Chen K, et al. Endocytosis of soluble immune complexes leads to their clearance by FcγRIIIB but induces neutrophil extracellular traps via FcγRIIA in vivo. Blood. 2012;120(22):4421–31.
pubmed: 22955924 pmcid: 3507149 doi: 10.1182/blood-2011-12-401133
Carmona-Rivera C, et al. Synovial fibroblast-neutrophil interactions promote pathogenic adaptive immunity in rheumatoid arthritis. Sci Immunol. 2017;2(10). https://doi.org/10.1126/sciimmunol.aag3358 .
Denny MF, et al. A distinct subset of proinflammatory neutrophils isolated from patients with systemic lupus erythematosus induces vascular damage and synthesizes type I IFNs. J Immunol. 2010;184(6):3284–97.
pubmed: 20164424 doi: 10.4049/jimmunol.0902199
Lood C, et al. Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease. Nat Med. 2016;22(2):146–53.
pubmed: 26779811 pmcid: 4742415 doi: 10.1038/nm.4027
Zhang S, et al. Abnormally increased low-density granulocytes in peripheral blood mononuclear cells are associated with interstitial lung disease in dermatomyositis. Mod Rheumatol. 2017;27(1):122–9.
pubmed: 27171278 doi: 10.1080/14397595.2016.1179861
Mukae H, et al. Clinical differences between interstitial lung disease associated with clinically amyopathic dermatomyositis and classic dermatomyositis. Chest. 2009;136(5):1341–7.
pubmed: 19581351 doi: 10.1378/chest.08-2740
Gerami P, et al. A systematic review of adult-onset clinically amyopathic dermatomyositis (dermatomyositis siné myositis): a missing link within the spectrum of the idiopathic inflammatory myopathies. J Am Acad Dermatol. 2006;54(4):597–613.
pubmed: 16546580 doi: 10.1016/j.jaad.2005.10.041
Baker MC, Chung L, Fiorentino DF. A mortality risk score model for clinically amyopathic dermatomyositis-associated interstitial lung disease: will it have the necessary “FLAIR” to improve clinical outcomes? Chest. 2020;158(4):1307–9.
pubmed: 33036075 doi: 10.1016/j.chest.2020.06.001
Liu L, et al. Promising neutrophil-associated biomarkers in lung diseases of patients with antisynthetase syndrome and dermatomyositis. J Immunol Res. 2022;2022:1886083.
pubmed: 36199667 pmcid: 9529515 doi: 10.1155/2022/1886083
Schnabel A, et al. Interstitial lung disease in polymyositis and dermatomyositis: clinical course and response to treatment. Semin Arthritis Rheum. 2003;32(5):273–84.
pubmed: 12701038 doi: 10.1053/sarh.2002.50012
Fujisawa T, et al. Prognostic factors for myositis-associated interstitial lung disease. PLoS ONE. 2014;9(6):e98824.
pubmed: 24905449 pmcid: 4048238 doi: 10.1371/journal.pone.0098824
Chino H, et al. Radiological and pathological correlation in Anti-MDA5 antibody-positive interstitial lung disease: rapidly progressive perilobular opacities and diffuse alveolar damage. Intern Med. 2016;55(16):2241–6.
pubmed: 27523002 doi: 10.2169/internalmedicine.55.5774
Sakamoto N, et al. Elevated alpha-defensin levels in plasma and bronchoalveolar lavage fluid from patients with myositis-associated interstitial lung disease. BMC Pulm Med. 2018;18(1):44.
pubmed: 29530007 pmcid: 5848598 doi: 10.1186/s12890-018-0609-5
Gono T, et al. Cytokine profiles in polymyositis and dermatomyositis complicated by rapidly progressive or chronic interstitial lung disease. Rheumatology. 2014;53(12):2196–203.
pubmed: 24970922 doi: 10.1093/rheumatology/keu258
Matsuda S, et al. Exploration of pathomechanism using comprehensive analysis of serum cytokines in polymyositis/dermatomyositis-interstitial lung disease. Rheumatology (Oxford). 2020;59(2):310–8.
pubmed: 31321420 doi: 10.1093/rheumatology/kez301
Chen X, et al. Neutrophil extracellular trapping network promotes the pathogenesis of neutrophil-associated asthma through macrophages. Immunol Invest. 2021;50(5):544–61.
pubmed: 32552227 doi: 10.1080/08820139.2020.1778720
Peng Y, et al. Neutrophil extracellular traps may contribute to interstitial lung disease associated with anti-MDA5 autoantibody positive dermatomyositis. Clin Rheumatol. 2018;37(1):107–15.
pubmed: 28842784 doi: 10.1007/s10067-017-3799-y
Garcia-Romo GS, et al. Netting neutrophils are major inducers of type I IFN production in pediatric systemic lupus erythematosus. Sci Transl Med. 2011;3(73):73ra20.
pubmed: 21389264 pmcid: 3143837 doi: 10.1126/scitranslmed.3001201
Lande R, et al. Neutrophils activate plasmacytoid dendritic cells by releasing self-DNA-peptide complexes in systemic lupus erythematosus. Sci Transl Med. 2011;3(73):73ra19.
pubmed: 21389263 pmcid: 3399524 doi: 10.1126/scitranslmed.3001180
Caudrillier A, et al. Platelets induce neutrophil extracellular traps in transfusion-related acute lung injury. J Clin Invest. 2012;122(7):2661–71.
pubmed: 22684106 pmcid: 3386815 doi: 10.1172/JCI61303
Saffarzadeh M, et al. Neutrophil extracellular traps directly induce epithelial and endothelial cell death: a predominant role of histones. PLoS ONE. 2012;7(2):e32366.
pubmed: 22389696 pmcid: 3289648 doi: 10.1371/journal.pone.0032366
Danoff SK, Casciola-Rosen L. The lung as a possible target for the immune reaction in myositis. Arthritis Res Ther. 2011;13(4):230.
pubmed: 21787440 pmcid: 3239334 doi: 10.1186/ar3347
Cheng OZ, Palaniyar N. NET balancing: a problem in inflammatory lung diseases. Front Immunol. 2013;4:1.
pubmed: 23355837 pmcid: 3553399 doi: 10.3389/fimmu.2013.00001
Zhang S, et al. Neutrophil extracellular traps activate lung fibroblast to induce polymyositis-related interstitial lung diseases via TLR9-miR-7-Smad2 pathway. J Cell Mol Med. 2020;24(2):1658–69.
pubmed: 31821687 doi: 10.1111/jcmm.14858
Kolahian S, et al. Immune mechanisms in pulmonary fibrosis. Am J Respir Cell Mol Biol. 2016;55(3):309–22.
pubmed: 27149613 doi: 10.1165/rcmb.2016-0121TR
Hinz B, et al. Recent developments in myofibroblast biology: paradigms for connective tissue remodeling. Am J Pathol. 2012;180(4):1340–55.
pubmed: 22387320 pmcid: 3640252 doi: 10.1016/j.ajpath.2012.02.004
Torres-Ruiz J, et al. Inflammatory myopathies and beyond: the dual role of neutrophils in muscle damage and regeneration. Front Immunol. 2023;14:1113214.
pubmed: 36923415 pmcid: 10008923 doi: 10.3389/fimmu.2023.1113214
Suzuki K, et al. Tissue accumulation of neutrophil extracellular traps mediates muscle hyperalgesia in a mouse model. Sci Rep. 2022;12(1):4136.
pubmed: 35264677 pmcid: 8907237 doi: 10.1038/s41598-022-07916-8
Liu L, et al. Induction of neutrophil extracellular traps during tissue injury: involvement of STING and toll-like receptor 9 pathways. Cell Prolif. 2020;53(10):e12775.
pubmed: 33079421 pmcid: 7574867 doi: 10.1111/cpr.12775
Seto N, et al. Neutrophil dysregulation is pathogenic in idiopathic inflammatory myopathies. JCI Insight. 2020;5(3). https://doi.org/10.1172/jci.insight.134189 .
Rodríguez-Carrio J, et al. Association between type I interferon pathway activation and clinical outcomes in rheumatic and musculoskeletal diseases: a systematic literature review informing EULAR points to consider. RMD Open. 2023;9(1):e002864.
pubmed: 36882218 pmcid: 10008483 doi: 10.1136/rmdopen-2022-002864
Tidball JG, Villalta SA. Regulatory interactions between muscle and the immune system during muscle regeneration. Am J Physiol Regul Integr Comp Physiol. 2010;298(5):R1173-87.
pubmed: 20219869 pmcid: 2867520 doi: 10.1152/ajpregu.00735.2009
Silvestre-Roig C, et al. Externalized histone H4 orchestrates chronic inflammation by inducing lytic cell death. Nature. 2019;569(7755):236–40.
pubmed: 31043745 pmcid: 6716525 doi: 10.1038/s41586-019-1167-6
Carmona-Rivera C, et al. Neutrophil extracellular traps induce endothelial dysfunction in systemic lupus erythematosus through the activation of matrix metalloproteinase-2. Ann Rheum Dis. 2015;74(7):1417–24.
pubmed: 24570026 doi: 10.1136/annrheumdis-2013-204837
Carlucci PM, et al. Neutrophil subsets and their gene signature associate with vascular inflammation and coronary atherosclerosis in lupus. JCI Insight. 2018;3(8). https://doi.org/10.1172/jci.insight.99276 .
doi: 10.1172/jci.insight.99276 pubmed: 29669944 pmcid: 5931124
Eimer MJ, et al. Clinical status and cardiovascular risk profile of adults with a history of juvenile dermatomyositis. J Pediatr. 2011;159(5):795–801.
pubmed: 21784434 pmcid: 3193560 doi: 10.1016/j.jpeds.2011.05.015
Warnatsch A, et al. Inflammation. Neutrophil extracellular traps license macrophages for cytokine production in atherosclerosis. Science. 2015;349(6245):316–20.
pubmed: 26185250 pmcid: 4854322 doi: 10.1126/science.aaa8064
Schauer C, et al. Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines. Nat Med. 2014;20(5):511–7.
pubmed: 24784231 doi: 10.1038/nm.3547
Lood C, et al. Platelet-derived S100A8/A9 and cardiovascular disease in systemic lupus erythematosus. Arthritis Rheumatol. 2016;68(8):1970–80.
pubmed: 26946461 doi: 10.1002/art.39656
Sato S, et al. Autoantibodies to a 140-kd polypeptide, CADM-140, in Japanese patients with clinically amyopathic dermatomyositis. Arthritis Rheum. 2005;52(5):1571–6.
pubmed: 15880816 doi: 10.1002/art.21023
Koga T, et al. The diagnostic utility of anti-melanoma differentiation-associated gene 5 antibody testing for predicting the prognosis of Japanese patients with DM. Rheumatology (Oxford). 2012;51(7):1278–84.
pubmed: 22378718 doi: 10.1093/rheumatology/ker518
Chen Z, et al. Utility of anti-melanoma differentiation-associated gene 5 antibody measurement in identifying patients with dermatomyositis and a high risk for developing rapidly progressive interstitial lung disease: a review of the literature and a meta-analysis. Arthritis Care Res (Hoboken). 2013;65(8):1316–24.
pubmed: 23908005 doi: 10.1002/acr.21985
Tournadre A, Miossec P. A critical role for immature muscle precursors in myositis. Nat Rev Rheumatol. 2013;9(7):438–42.
pubmed: 23478496 doi: 10.1038/nrrheum.2013.26
Kessenbrock K, et al. Netting neutrophils in autoimmune small-vessel vasculitis. Nat Med. 2009;15(6):623–5.
pubmed: 19448636 pmcid: 2760083 doi: 10.1038/nm.1959
Zhao L, et al. Machine learning algorithms identify clinical subtypes and cancer in anti-TIF1γ + myositis: a longitudinal study of 87 patients. Front Immunol. 2022;13:802499.
pubmed: 35237262 pmcid: 8883045 doi: 10.3389/fimmu.2022.802499
Owen CA, Campbell EJ. The cell biology of leukocyte-mediated proteolysis. J Leukoc Biol. 1999;65(2):137–50.
pubmed: 10088596 doi: 10.1002/jlb.65.2.137
Wu S, et al. Correlation of PMN elastase and PMN elastase-to-neutrophil ratio with disease activity in patients with myositis. J Transl Med. 2019;17(1):420.
pubmed: 31842908 pmcid: 6912949 doi: 10.1186/s12967-019-02176-z
Carden D, et al. Neutrophil elastase promotes lung microvascular injury and proteolysis of endothelial cadherins. Am J Physiol. 1998;275(2):H385-92.
pubmed: 9683424
Ionescu CV, et al. Neutrophils induce sequential focal changes in endothelial adherens junction components: role of elastase. Microcirculation. 2003;10(2):205–20.
pubmed: 12700588 doi: 10.1038/sj.mn.7800185
Chua F, Laurent GJ. Neutrophil elastase: mediator of extracellular matrix destruction and accumulation. Proc Am Thorac Soc. 2006;3(5):424–7.
pubmed: 16799086 doi: 10.1513/pats.200603-078AW
Ferry G, et al. Activation of MMP-9 by neutrophil elastase in an in vivo model of acute lung injury. FEBS Lett. 1997;402(2–3):111–5.
pubmed: 9037177 doi: 10.1016/S0014-5793(96)01508-6
Wang S, et al. PECAM-1, alpha6 integrins and neutrophil elastase cooperate in mediating neutrophil transmigration. J Cell Sci. 2005;118(Pt 9):2067–76.
pubmed: 15840647 doi: 10.1242/jcs.02340
Wang J. Neutrophils in tissue injury and repair. Cell Tissue Res. 2018;371(3):531–9.
pubmed: 29383445 pmcid: 5820392 doi: 10.1007/s00441-017-2785-7
D’Alessandro M, et al. Neutrophil-to-lymphocyte ratio in bronchoalveolar lavage from IPF patients: a novel prognostic biomarker? Minerva Med. 2022;113(3):526–31.
pubmed: 32407050
Gregory AD, et al. Neutrophil elastase promotes myofibroblast differentiation in lung fibrosis. J Leukoc Biol. 2015;98(2):143–52.
pubmed: 25743626 pmcid: 4763951 doi: 10.1189/jlb.3HI1014-493R
Arecco N, et al. Elastase levels and activity are increased in dystrophic muscle and impair myoblast cell survival, proliferation and differentiation. Sci Rep. 2016;6:24708.
pubmed: 27241590 pmcid: 4886533 doi: 10.1038/srep24708
Gao S, et al. The roles of neutrophil serine proteinases in idiopathic inflammatory myopathies. Arthritis Res Ther. 2018;20(1):134.
pubmed: 29976235 pmcid: 6034343 doi: 10.1186/s13075-018-1632-x
Urban CF, et al. Neutrophil extracellular traps contain calprotectin, a cytosolic protein complex involved in host defense against Candida albicans. PLoS Pathog. 2009;5(10):e1000639.
pubmed: 19876394 pmcid: 2763347 doi: 10.1371/journal.ppat.1000639
Xu J, et al. Extracellular histones are major mediators of death in sepsis. Nat Med. 2009;15(11):1318–21.
pubmed: 19855397 pmcid: 2783754 doi: 10.1038/nm.2053
Tsourouktsoglou TD, et al. Histones, DNA, and citrullination promote neutrophil extracellular trap inflammation by regulating the localization and activation of TLR4. Cell Rep. 2020;31(5):107602.
pubmed: 32375035 doi: 10.1016/j.celrep.2020.107602
Shrestha B, et al. Recombinant thrombomodulin suppresses histone-induced neutrophil extracellular trap formation. Front Immunol. 2019;10:2535.
pubmed: 31736962 pmcid: 6828967 doi: 10.3389/fimmu.2019.02535
Hsieh IN, et al. Histone H4 directly stimulates neutrophil activation through membrane permeabilization. J Leukoc Biol. 2021;109(4):763–75.
pubmed: 32803840 doi: 10.1002/JLB.3A0620-342R
Rohrbach AS, et al. Activation of PAD4 in NET formation. Front Immunol. 2012;3:360.
pubmed: 23264775 pmcid: 3525017 doi: 10.3389/fimmu.2012.00360
Suzuki M, et al. PAD4 deficiency improves bleomycin-induced neutrophil extracellular traps and fibrosis in mouse lung. Am J Respir Cell Mol Biol. 2020;63(6):806–18.
pubmed: 32915635 doi: 10.1165/rcmb.2019-0433OC
Chapuy-Regaud S, et al. Fibrin deimination in synovial tissue is not specific for rheumatoid arthritis but commonly occurs during synovitides. J Immunol. 2005;174(8):5057–64.
pubmed: 15814737 doi: 10.4049/jimmunol.174.8.5057
Makrygiannakis D, et al. Citrullination is an inflammation-dependent process. Ann Rheum Dis. 2006;65(9):1219–22.
pubmed: 16540548 pmcid: 1798285 doi: 10.1136/ard.2005.049403
Wang W, Peng W, Wu S. Low serum level of citrullinated histone H3 in patients with dermatomyositis. J Clin Lab Anal. 2023;37(6):e24876.
pubmed: 37003600 pmcid: 10156100 doi: 10.1002/jcla.24876
Samara KD, et al. Upregulation of citrullination pathway: from autoimmune to idiopathic lung fibrosis. Respir Res. 2017;18(1):218.
pubmed: 29287593 pmcid: 5747943 doi: 10.1186/s12931-017-0692-9
Negreros M, Flores-Suarez LF. A proposed role of neutrophil extracellular traps and their interplay with fibroblasts in ANCA-associated vasculitis lung fibrosis. Autoimmun Rev. 2021;20(4):102781.
pubmed: 33609801 doi: 10.1016/j.autrev.2021.102781
Chow OA, et al. Statins enhance formation of phagocyte extracellular traps. Cell Host Microbe. 2010;8(5):445–54.
pubmed: 21075355 pmcid: 3008410 doi: 10.1016/j.chom.2010.10.005
Kahlenberg JM, Kaplan MJ. Little peptide, big effects: the role of LL-37 in inflammation and autoimmune disease. J Immunol. 2013;191(10):4895–901.
pubmed: 24185823 doi: 10.4049/jimmunol.1302005
van de Vlekkert J, Hoogendijk JE, de Visser M. Long-term follow-up of 62 patients with myositis. J Neurol. 2014;261(5):992–8.
pubmed: 24658663 doi: 10.1007/s00415-014-7313-z
Lim J, et al. Intravenous immunoglobulins as first-line treatment in idiopathic inflammatory myopathies: a pilot study. Rheumatology (Oxford). 2021;60(4):1784–92.
pubmed: 33099648 doi: 10.1093/rheumatology/keaa459
Ichiyasu H, et al. Favorable outcome with hemoperfusion of polymyxin B-immobilized fiber column for rapidly progressive interstitial pneumonia associated with clinically amyopathic dermatomyositis: report of three cases. Mod Rheumatol. 2014;24(2):361–5.
pubmed: 24593215 doi: 10.3109/14397595.2013.852847
Fousert E, Toes R, Desai J. Neutrophil extracellular traps (NETs) take the central stage in driving autoimmune responses. Cells. 2020;9(4):915.
pubmed: 32276504 pmcid: 7226846 doi: 10.3390/cells9040915
Galeotti C, Kaveri SV, Bayry J. IVIG-mediated effector functions in autoimmune and inflammatory diseases. Int Immunol. 2017;29(11):491–8.
pubmed: 28666326 doi: 10.1093/intimm/dxx039
Opinc AH, Makowska JS. Antisynthetase syndrome - much more than just a myopathy. Semin Arthritis Rheum. 2021;51(1):72–83.
pubmed: 33360231 doi: 10.1016/j.semarthrit.2020.09.020

Auteurs

Ruiting Liu (R)

Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.

Hongjiang Liu (H)

Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.

Leiyi Yang (L)

Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.

Changpei Li (C)

Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.

Geng Yin (G)

Health Management Center, General Practice Medical Center, West China Hospital, Sichuan University, Chengdu, China. yingeng1975@163.com.

Qibing Xie (Q)

Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China. xieqibing1971@163.com.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH