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Therapeutic ACPA inhibits NET formation: a potential therapy for neutrophil-mediated inflammatory diseases

Cellular & Molecular Immunology 2021年第6期18卷 1528-1544页

作者： Renato G.S.Chirivi Jos W.gvan Rosmalen Maarten van der Linden Maximilien Euler Gonny Schmets Galina Bogatkevich Konstantinos Kambas Jonas hahn Quinte Braster Oliver Soehnlein Markus h.hoffmann helmuth h.gvan es Jos M.h.Raats ModiQuest B.V. OssThe Netherlands Citryll B.V. OssThe Netherlands Department of Internal Medicine 3-Rheumatology and Immunology University Hospital ErlangenFriedrich-Alexander-Universität Erlangen-Nürnberg and University Hospital ErlangenErlangenGermany Department of Medicine Division of Rheumatology and ImmunologyMedical University of South CarolinaCharlestonSCUSA Laboratory of Molecular hematology Democritus University of ThraceAlexandroupoliGreece Institute for Cardiovascular Prevention(IPEK) Ludwig-Maximilians-University MunichMunichGermany German Center for Cardiovascular Research(DZhK) Partner Site Munich Heart AllianceMunichGermany Department of Physiology and Pharmacology Karolinska InstitutetStockholmSweden

Excessive release of neutrophil extracellular traps(NETs)is associated with disease severity and contributes to tissue injury,followed by severe organ *** or genetic inhibition of NET release reduces pathology in multiple inflammatory disease models,indicating that NETs are potential therapeutic ***,we demonstrate using a preclinical basket approach that our therapeutic anti-citrullinated protein antibody(tACPA)has broad therapeutic *** with tACPA prevents disease symptoms in various mouse models with plausible NET-mediated pathology,including inflammatory arthritis(IA),pulmonary fibrosis,inflammatory bowel disease and *** show that citrulline residues in the N-termini of histones 2A and 4 are specific targets for therapeutic intervention,whereas antibodies against other N-terminal post-translational histone modifications have no therapeutic *** citrullinated histones are generated during NET release,we investigated the ability of tACPA to inhibit NET *** suppressed NET release from human neutrophils triggered with physiologically relevant human disease-related ***,tACPA diminished NET release and potentially initiated NET uptake by macrophages in vivo,which was associated with reduced tissue damage in the joints of a chronic arthritis mouse model of *** our knowledge,we are the first to describe an antibody with NET-inhibiting properties and thereby propose tACPA as a drug candidate for NET-mediated inflammatory diseases,as it eliminates the noxious triggers that lead to continued inflammation and tissue damage in a multidimensional manner.

关键词： Neutrophil Extracellular Traps Autoimmunity Citrullination Therapeutic Antibody NET inhibition

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