Autoimmune, rheumatic, chronic inflammatory diseases: Neutrophil extracellular traps on parade

References

• Lleo A, Invernizzi P, Gao B, et al. Definition of human autoimmunity–autoantibodies versus autoimmune disease. Autoimmun Rev. 2010;9:A259–A266.
   PubMed Web of Science ®Google Scholar
• Hayter SM, Cook MC. Updated assessment of the prevalence, spectrum and case definition of autoimmune disease. Autoimmun Rev. 2012;11:754–765.
   PubMed Web of Science ®Google Scholar
• Gaipl US, Munoz LE, Grossmayer G, et al. Clearance deficiency and systemic lupus erythematosus (SLE). J Autoimmun. 2007;28:114–121.
   PubMed Web of Science ®Google Scholar
• Munoz LE, Herrmann M, Berens C. Dying autologous cells as instructors of the immune system. Clin Exp Immunol. 2015;179:1–4.
   PubMed Web of Science ®Google Scholar
• Mahajan A, Herrmann M, Munoz LE. Clearance deficiency and cell death pathways: A model for the pathogenesis of SLE. Front Immunol. 2016;7:35.
   PubMed Web of Science ®Google Scholar
• Muñoz LE, Lauber K, Schiller M, et al. The role of defective clearance of apoptotic cells in systemic autoimmunity. Nat Rev Rheumatol. 2010;6:280–289.
   PubMed Web of Science ®Google Scholar
• Brinkmann V, Reichard U, Goosmann C, et al. Neutrophil extracellular traps kill bacteria. Science. 2004;303:1532–1535.
   PubMed Web of Science ®Google Scholar
• Biermann MHC, Podolska MJ, Knopf J, et al. Oxidative burst-dependent NETosis is implicated in the resolution of necrosis-associated sterile inflammation. Front Immunol. 2016;7:557.
   PubMed Web of Science ®Google Scholar
• Munoz LE, Bilyy R, Biermann MH, et al. Nanoparticles size-dependently initiate self-limiting NETosis-driven inflammation. Proc Natl Acad Sci USA. 2016;113:E5856–E5865.
   PubMed Web of Science ®Google Scholar
• Muñoz LE, Leppkes M, Fuchs TA, et al. Missing in action – the meaning of cell death in tissue damage and inflammation. Immunol Rev. 2017;280:26–40.
   PubMed Web of Science ®Google Scholar
• Ermert D, Zychlinsky A, Urban C. Fungal and bacterial killing by neutrophils. Methods Mol Biol. 2009;470:293–312.
   PubMedGoogle Scholar
• Manfredi AA, Ramirez GA, Rovere-Querini P, et al. The neutrophil's choice: phagocytose vs make neutrophil extracellular traps. Front Immunol. 2018;9:288.
   PubMed Web of Science ®Google Scholar
• Yipp BG, Kubes P. NETosis: how vital is it? Blood. 2013;122:2784–2794.
   PubMed Web of Science ®Google Scholar
• Silvestre-Roig C, Hidalgo A, Soehnlein O. Neutrophil heterogeneity: implications for homeostasis and pathogenesis. Blood. 2016;127:2173–2181.
   PubMed Web of Science ®Google Scholar
• Leppkes M, Maueröder C, Hirth S, et al. Externalized decondensed neutrophil chromatin occludes pancreatic ducts and drives pancreatitis. Nat Comms. 2016;7:10973.
   PubMed Web of Science ®Google Scholar
• Zawrotniak M, Bochenska O, Karkowska-Kuleta J, et al. Aspartic proteases and major cell wall components in candida albicans trigger the release of neutrophil extracellular traps. Front Cell Infect Microbiol. 2017;7:414.
   PubMed Web of Science ®Google Scholar
• Desai J, Foresto-Neto O, Honarpisheh M, et al. Particles of different sizes and shapes induce neutrophil necroptosis followed by the release of neutrophil extracellular trap-like chromatin. Sci Rep. 2017;7:15003.
   PubMed Web of Science ®Google Scholar
• Schauer C, Janko C, Munoz LE, et al. Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines. Nat Med. 2014;20:511–517.
   PubMed Web of Science ®Google Scholar
• Bilyy R, Fedorov V, Vovk V, et al. Neutrophil extracellular traps form a barrier between necrotic and viable areas in acute abdominal inflammation. Front Immunol. 2016;7:424.
   PubMed Web of Science ®Google Scholar
• Reinwald C, Schauer C, Csepregi JZ, et al. Erratum: reply to “Neutrophils are not required for resolution of acute gouty arthritis in mice”. Nat Med. 2017;23:526.
   PubMed Web of Science ®Google Scholar
• Hakkim A, Fürnrohr BG, Amann K, et al. Impairment of neutrophil extracellular trap degradation is associated with lupus nephritis. Proc Natl Acad Sci USA. 2010;107:9813–9818.
   PubMed Web of Science ®Google Scholar
• Jiménez-Alcázar M, Rangaswamy C, Panda R, et al. Host DNases prevent vascular occlusion by neutrophil extracellular traps. Science. 2017;358:1202–1206.
   PubMed Web of Science ®Google Scholar
• Knight JS, Carmona-Rivera C, Kaplan MJ. Proteins derived from neutrophil extracellular traps may serve as self-antigens and mediate organ damage in autoimmune diseases. Front Immun. 2012;3:380.
   PubMed Web of Science ®Google Scholar
• Soderberg D, Segelmark M. Neutrophil extracellular traps in ANCA-associated vasculitis. Front Immunol. 2016;7:256.
   PubMed Web of Science ®Google Scholar
• Bouts YM, Wolthuis DFGJ, Dirkx MFM, et al. Apoptosis and NET formation in the pathogenesis of SLE. Autoimmunity. 2012;45:597–601.
   PubMed Web of Science ®Google Scholar
• Pradhan VD, Badakere SS, Bichile LS, et al. Anti-neutrophil cytoplasmic antibodies (ANCA) in systemic lupus erythematosus: prevalence, clinical associations and correlation with other autoantibodies. J Assoc Physicians India. 2004;52:533–537.
   PubMedGoogle Scholar
• Burlingame RW, Boey ML, Starkebaum G, et al. The central role of chromatin in autoimmune responses to histones and DNA in systemic lupus erythematosus. J Clin Invest. 1994;94:184–192.
   PubMed Web of Science ®Google Scholar
• Yeh T-M, Chang H-C, Liang C-C, et al. Deoxyribonuclease-inhibitory antibodies in systemic lupus erythematosus. J Biomed Sci. 2003;10:544–551.
   PubMed Web of Science ®Google Scholar
• Emlen W, Ansari R, Burdick G. DNA-anti-DNA immune complexes. Antibody protection of a discrete DNA fragment from DNase digestion in vitro. J Clin Invest. 1984;74:185–190.
   PubMed Web of Science ®Google Scholar
• Villanueva E, Yalavarthi S, Berthier CC, et al. Netting neutrophils induce endothelial damage, infiltrate tissues, and expose immunostimulatory molecules in systemic lupus erythematosus. J Immunol. 2011;187:538–552.
   PubMed Web of Science ®Google Scholar
• Denny MF, Yalavarthi S, Zhao W, 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;184:3284–3297.
   PubMed Web of Science ®Google Scholar
• Baechler EC, Batliwalla FM, Karypis G, et al. Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus. Proc Natl Acad Sci USA. 2003;100:2610–2615.
   PubMed Web of Science ®Google Scholar
• Lande R, Ganguly D, Facchinetti V, et al. Neutrophils activate plasmacytoid dendritic cells by releasing self-DNA-peptide complexes in systemic lupus erythematosus. Sci Transl Med. 2011;3:73ra19.
   PubMed Web of Science ®Google Scholar
• Garcia-Romo GS, Caielli S, Vega B, et al. Netting neutrophils are major inducers of type I IFN production in pediatric systemic lupus erythematosus. Sci Transl Med. 2011;3:73ra20.
   PubMed Web of Science ®Google Scholar
• Kahlenberg JM, Carmona-Rivera C, Smith CK, et al. Neutrophil extracellular trap-associated protein activation of the NLRP3 inflammasome is enhanced in lupus macrophages. J Immunol. 2013;190:1217–1226.
   PubMed Web of Science ®Google Scholar
• Kahlenberg JM, Thacker SG, Berthier CC, et al. Inflammasome activation of IL-18 results in endothelial progenitor cell dysfunction in systemic lupus erythematosus. J Immunol. 2011;187:6143–6156.
   PubMed Web of Science ®Google Scholar
• Calvani N, Richards HB, Tucci M, et al. Up-regulation of IL-18 and predominance of a Th1 immune response is a hallmark of lupus nephritis. Clin Exp Immunol. 2004;138:171–178.
   PubMed Web of Science ®Google Scholar
• Mitroulis I, Kambas K, Chrysanthopoulou A, et al. Neutrophil extracellular trap formation is associated with IL-1β and autophagy-related signaling in gout. PLoS One. 2011;6: e29318.
   PubMed Web of Science ®Google Scholar
• Chen H-H, Huang N, Chen Y-M, et al. Association between a history of periodontitis and the risk of rheumatoid arthritis: a nationwide, population-based, case-control study. Ann Rheum Dis. 2013;72:1206–1211.
   PubMed Web of Science ®Google Scholar
• Maresz KJ, Hellvard A, Sroka A, et al. Porphyromonas gingivalis facilitates the development and progression of destructive arthritis through its unique bacterial peptidylarginine deiminase (PAD). PLoS Pathog. 2013;9:e1003627.
   PubMed Web of Science ®Google Scholar
• Quirke A-M, Lugli EB, Wegner N, et al. Heightened immune response to autocitrullinated Porphyromonas gingivalis peptidylarginine deiminase: a potential mechanism for breaching immunologic tolerance in rheumatoid arthritis. Ann Rheum Dis. 2014;73:263–269.
   PubMed Web of Science ®Google Scholar
• Makrygiannakis D, Hermansson M, Ulfgren A-K, et al. Smoking increases peptidylarginine deiminase 2 enzyme expression in human lungs and increases citrullination in BAL cells. Ann Rheum Dis. 2008;67:1488–1492.
   PubMed Web of Science ®Google Scholar
• McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med. 2011;365:2205–2219.
   PubMed Web of Science ®Google Scholar
• Lugli EB, Correia R, Fischer R, et al. Expression of citrulline and homocitrulline residues in the lungs of non-smokers and smokers: implications for autoimmunity in rheumatoid arthritis. Arthritis Res Ther. 2015;17:9.
   PubMed Web of Science ®Google Scholar
• Hosseinzadeh A, Thompson PR, Segal BH, et al. Nicotine induces neutrophil extracellular traps. J Leukoc Biol. 2016;100:1105–1112.
   PubMed Web of Science ®Google Scholar
• Lee J, Luria A, Rhodes C, et al. Nicotine drives neutrophil extracellular traps formation and accelerates collagen-induced arthritis. Rheumatology (Oxford). 2017;56:644–653.
   PubMed Web of Science ®Google Scholar
• Sokolove J, Bromberg R, Deane KD, et al. Autoantibody epitope spreading in the pre-clinical phase predicts progression to rheumatoid arthritis. PLoS One. 2012;7: e35296.
   PubMed Web of Science ®Google Scholar
• Johansson L, Pratesi F, Brink M, et al. Antibodies directed against endogenous and exogenous citrullinated antigens pre-date the onset of rheumatoid arthritis. Arthritis Res Ther. 2016;18:127.
   PubMed Web of Science ®Google Scholar
• Corsiero E, Pratesi F, Prediletto E, et al. NETosis as source of autoantigens in rheumatoid arthritis. Front Immunol. 2016;7:485.
   PubMed Web of Science ®Google Scholar
• Demoruelle MK, Harrall KK, Ho L, et al. Anti-citrullinated protein antibodies are associated with neutrophil extracellular traps in the sputum in relatives of rheumatoid arthritis patients. Arthritis Rheumatol. 2017;69:1165–1175.
   PubMed Web of Science ®Google Scholar
• Demoruelle MK, Bowers E, Lahey LJ, et al. Antibody responses to citrullinated and noncitrullinated antigens in the sputum of subjects with rheumatoid arthritis and subjects at risk for development of rheumatoid arthritis. Arthritis Rheumatol. 2018;70:516–527.
   PubMed Web of Science ®Google Scholar
• Giles JT, Fert-Bober J, Park J, et al. Myocardial citrullination in rheumatoid arthritis: a correlative histopathologic study. Arthritis Res Ther. 2012;14: R39.
   PubMed Web of Science ®Google Scholar
• Neeli I, Khan SN, Radic M. Histone deimination as a response to inflammatory stimuli in neutrophils. J Immunol. 2008;180:1895–1902.
   PubMed Web of Science ®Google Scholar
• Wang Y, Li M, Stadler S, et al. Histone hypercitrullination mediates chromatin decondensation and neutrophil extracellular trap formation. J Cell Biol. 2009;184:205–213.
   PubMed Web of Science ®Google Scholar
• Pratesi F, Dioni I, Tommasi C, et al. Antibodies from patients with rheumatoid arthritis target citrullinated histone 4 contained in neutrophils extracellular traps. Ann Rheumat Dis. 2014;73:1414–1422.
   PubMed Web of Science ®Google Scholar
• Dwivedi N, Upadhyay J, Neeli I, et al. Felty's syndrome autoantibodies bind to deiminated histones and neutrophil extracellular chromatin traps. Arthritis Rheum. 2012;64:982–992.
   PubMedGoogle Scholar
• Corsiero E, Bombardieri M, Carlotti E, et al. Single cell cloning and recombinant monoclonal antibodies generation from RA synovial B cells reveal frequent targeting of citrullinated histones of NETs. Ann Rheum Dis. 2016;75:1866–1875.
   PubMed Web of Science ®Google Scholar
• Romero V, Fert-Bober J, Nigrovic PA, et al. Immune-mediated pore-forming pathways induce cellular hypercitrullination and generate citrullinated autoantigens in rheumatoid arthritis. Sci Transl Med. 2013;5:209ra150.
   PubMed Web of Science ®Google Scholar
• Khandpur R, Carmona-Rivera C, Vivekanandan-Giri A, et al. NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis. Sci Transl Med. 2013;5:178ra40.
   PubMed Web of Science ®Google Scholar
• Wang W, Peng W, Ning X. Increased levels of neutrophil extracellular trap remnants in the serum of patients with rheumatoid arthritis. Int J Rheum Dis. 2018;21:415–421.
   PubMed Web of Science ®Google Scholar
• Papadaki G, Kambas K, Choulaki C, et al. Neutrophil extracellular traps exacerbate Th1-mediated autoimmune responses in rheumatoid arthritis by promoting DC maturation. Eur J Immunol. 2016;46:2542–2554.
   PubMed Web of Science ®Google Scholar
• Jennette JC, Falk RJ, Bacon PA, et al. 2012 Revised International Chapel Hill consensus conference nomenclature of vasculitides. Arthritis Rheum. 2013;65:1–11.
   PubMed Web of Science ®Google Scholar
• Lamprecht P, Kerstein A, Klapa S, et al. Pathogenetic and clinical aspects of anti-neutrophil cytoplasmic autoantibody-associated vasculitides. Front Immunol. 2018;9:680.
   PubMed Web of Science ®Google Scholar
• Söderberg D, Kurz T, Motamedi A, et al. Increased levels of neutrophil extracellular trap remnants in the circulation of patients with small vessel vasculitis, but an inverse correlation to anti-neutrophil cytoplasmic antibodies during remission. Rheumatology (Oxford). 2015;54:2085–2094.
   PubMed Web of Science ®Google Scholar
• Grayson PC, Carmona-Rivera C, Xu L, 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;67:1922–1932.
   PubMed Web of Science ®Google Scholar
• Kessenbrock K, Krumbholz M, Schönermarck U, et al. Netting neutrophils in autoimmune small-vessel sel vasculitis. Nat Med. 2009;15:623–625.
   PubMed Web of Science ®Google Scholar
• Panda R, Krieger T, Hopf L, et al. Neutrophil extracellular traps contain selected antigens of anti-neutrophil cytoplasmic antibodies. Front Immunol. 2017;8:439.
   PubMed Web of Science ®Google Scholar
• Gupta S, Kaplan MJ. The role of neutrophils and NETosis in autoimmune and renal diseases. Nat Rev Nephrol. 2016;12:402–413.
   PubMed Web of Science ®Google Scholar
• Boeltz S, Muñoz LE, Fuchs TA, et al. Neutrophil extracellular traps open the Pandora's box in severe malaria. Front Immunol. 2017;8:874.
   PubMed Web of Science ®Google Scholar
• Bertolaccini ML, Amengual O, Andreoli L, et al. 14th International congress on antiphospholipid antibodies task force. Report on antiphospholipid syndrome laboratory diagnostics and trends. Autoimmun Rev. 2014;13:917–930.
   PubMed Web of Science ®Google Scholar
• Miyakis S, Lockshin MD, Atsumi T, et al. International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS). J Thromb Haemost. 2006;4:295–306.
   PubMed Web of Science ®Google Scholar
• Yalavarthi S, Gould TJ, Rao AN, et al. Release of neutrophil extracellular traps by neutrophils stimulated with antiphospholipid antibodies: a newly identified mechanism of thrombosis in the antiphospholipid syndrome. Arthritis Rheumatol. 2015;67:2990–3003.
   PubMed Web of Science ®Google Scholar
• Meng H, Yalavarthi S, Kanthi Y, et al. In vivo role of neutrophil extracellular traps in antiphospholipid antibody-mediated venous thrombosis. Arthritis Rheumatol. 2017;69:655–667.
   PubMed Web of Science ®Google Scholar
• Leffler J, Stojanovich L, Shoenfeld Y, et al. Degradation of neutrophil extracellular traps is decreased in patients with antiphospholipid syndrome. Clin Exp Rheumatol. 2014;32:66–70.
   PubMed Web of Science ®Google Scholar
• Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med. 2009;361:496–509.
   PubMed Web of Science ®Google Scholar
• Girolomoni G, Mrowietz U, Paul C. Psoriasis: rationale for targeting interleukin-17. Br J Dermatol. 2012;167:717–724.
   PubMed Web of Science ®Google Scholar
• Pfohler C, Muller CS, Vogt T. Psoriasis vulgaris and psoriasis pustulosa – epidemiology, quality of life, comorbidities and treatment. CRR. 2013;9:2–7.
   Google Scholar
• Naldi L, Mercuri SR. Epidemiology of comorbidities in psoriasis. Dermatol Ther. 2010;23:114–118.
   PubMed Web of Science ®Google Scholar
• Christophers E, Metzler G, Rocken M. Bimodal immune activation in psoriasis. Br J Dermatol. 2014;170:59–65.
   PubMed Web of Science ®Google Scholar
• Ganguly D, Chamilos G, Lande R, et al. Self-RNA-antimicrobial peptide complexes activate human dendritic cells through TLR7 and TLR8. J Exp Med. 2009;206:1983–1994.
   PubMed Web of Science ®Google Scholar
• Lande R, Gregorio J, Facchinetti V, et al. Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide. Nature. 2007;449:564–569.
   PubMed Web of Science ®Google Scholar
• Hu SC-S, Yu H-S, Yen F-L, et al. Neutrophil extracellular trap formation is increased in psoriasis and induces human β-defensin-2 production in epidermal keratinocytes. Sci Rep. 2016;6:31119.
   PubMed Web of Science ®Google Scholar
• Skrzeczynska-Moncznik J, Wlodarczyk A, Zabieglo K, et al. Secretory leukocyte proteinase inhibitor-competent DNA deposits are potent stimulators of plasmacytoid dendritic cells: implication for psoriasis. J Immunol. 2012;189:1611–1617.
   PubMed Web of Science ®Google Scholar
• Bley TA, Johnson KM, François CJ, et al. Noninvasive assessment of transstenotic pressure gradients in porcine renal artery stenoses by using vastly undersampled phase-contrast MR angiography. Radiology. 2011;261:266–273.
   PubMed Web of Science ®Google Scholar