title: Infections and antineutrophil cytoplasmic antibodies: triggering mechanisms.
abstract: The precise cause of the antineutrophil cytoplasmic antibodies (ANCA) autoimmunity is not known and is likely to be multifactorial. Infections may trigger formation of ANCA and a fraction of the patients with infection-triggered ANCA develop ANCA-associated vasculitis. Here we discuss some of the proposed mechanisms of ANCA formation during the course of infection. They include initiation of autoimmune response by microbial peptides that are complementary to autoantigens; epigenetic silencing and antigen complementarity leading to upregulation of autoantigen genes; molecular mimicry between bacterial and self-antigens; formation of neutrophil extracellular traps that stimulate immune processes including production of ANCA; and interaction of bacterial components with Toll-like receptors, which leads to formation of mediators affecting the immune responses to infections and can trigger ANCA production. Further work is needed to clarify these mechanisms and develop preventive measures and therapeutic interventions.
authors.affiliation: Division of Rheumatology, Department of Internal Medicine, University of New Mexico School of Medicine Health Sciences Center, Mail Stop MSC10-5550, Albuquerque, NM 87131, USA. Electronic address: kkonstantinov@salud.unm.edu.
authors.forename: Konstantin N
authors.initials: KN
authors.lastname: Konstantinov
authors.affiliation: Department of Infectious Diseases and Rheumatology, Rigshospitalet, Copenhagen, University Hospital, Blegdamsvej 9, DK-2100 Denmark. Electronic address: constance.jensina.ulff-moeller@regionh.dk.
authors.forename: Constance J
authors.initials: CJ
authors.lastname: Ulff-Møller
authors.affiliation: Section of Nephrology, Raymond G. Murphy Veterans Affairs Medical Center and University of New Mexico School of Medicine, Renal Section, VA Medical Center, 1501 San Pedro, SE, Albuquerque, NM 87108, USA. Electronic address: Antonios.Tzamaloukas@va.gov.
authors.forename: Antonios H
authors.initials: AH
authors.lastname: Tzamaloukas
mesh_terms: D000818:Animals; D019268:Antibodies, Antineutrophil Cytoplasmic / Q000276:immunology*; D001324:Autoantigens / Q000276:immunology; D044127:Epigenesis, Genetic; D006801:Humans; D007239:Infections / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology
chemical_list: D019268:Antibodies, Antineutrophil Cytoplasmic; D001324:Autoantigens; D051193:Toll-Like Receptors