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dc.contributor.authorVærøy, Henning
dc.contributor.authorAdori, Csaba
dc.contributor.authorLegrand, Romain
dc.contributor.authorLucas, Nicolas
dc.contributor.authorBreton, Jonathan
dc.contributor.authorCottard, Caroline
dc.contributor.authordo Rego, Jean-Claude
dc.contributor.authorDuparc, Céline
dc.contributor.authorLouiset, Estelle
dc.contributor.authorLefebvre, Hervé
dc.contributor.authorDéchelotte Pierre
dc.contributor.authorWestern, Elin
dc.contributor.authorAndersson, Stein
dc.contributor.authorHökfelt, Tomas
dc.contributor.authorFetissov, Sergueï O
dc.date.accessioned2019-07-23T07:50:20Z
dc.date.available2019-07-23T07:50:20Z
dc.date.issued2018-06-25
dc.identifier.citationVærøy, H., Adori, C., Legrand, R., Lucas, N., Breton, J., Cottard, C., ... & Déchelotte, P. (2018). Autoantibodies reactive to adrenocorticotropic hormone can alter cortisol secretion in both aggressive and nonaggressive humans. Proceedings of the National Academy of Sciences, 115(28), E6576-E6584.en
dc.identifier.issn0027-8424
dc.identifier.urihttps://hdl.handle.net/10642/7331
dc.description.abstractViolent aggression in humans may involve a modified response to stress, but the underlying mechanisms are not well understood. Here we show that naturally present autoantibodies reactive to adrenocorticotropic hormone (ACTH) exhibit distinct epitope-binding profiles to ACTH peptide in subjects with a history of violent aggression compared with controls. Namely, while nonaggressive male controls displayed a preferential IgG binding to the ACTH central part (amino acids 11–24), subjects who had committed violent acts of aggression had IgG with increased affinity to ACTH, preferentially binding to its N terminus (amino acids 1–13). Purified IgGs from approximately half of the examined sera were able to block ACTH-induced cortisol secretion of human adrenal cells in vitro, irrespective of the source of sample (from a control subject or a violent aggressor). Nevertheless, in the resident–intruder test in mice, i.p. injection of residents with ACTH and IgG from aggressive subjects, but not from control subjects, shortened latency for the first attack against intruders. Immunohistochemical screening of violent aggressors’ sera on rat brain and pituitary sections did not show IgG binding to ACTH-producing cells, but 4 of 16 sera revealed selective binding to a nonidentified antigen in vasopressinergic neurons of the hypothalamic paraventricular and supraoptic nuclei. Thus, the data show that ACTH-reactive plasmatic IgGs exhibit differential epitope preference in control and violently aggressive subjects. These IgGs can modulate ACTH-induced cortisol secretion and, hence, are involved in the regulation of the stress response. However, the possible role of ACTH-reactive autoantibodies in aggressive behavior needs further investigation.en
dc.language.isoenen
dc.relation.ispartofseriesProceedings of the National Academy of Sciences;115(28)
dc.rightsAttribution-NonCommercial 3.0 United States This is an open access article, originally published at https://doi.org/10.1073/pnas.1720008115en
dc.rights.urihttp://creativecommons.org/licenses/by-nc/3.0/us/*
dc.subjectArtikkelen
dc.subjectVDP::Medisinske Fag: 700en
dc.titleAutoantibodies reactive to adrenocorticotropic hormone can alter cortisol secretion in both aggressive and nonaggressive humansen
dc.typeJournal articleen
dc.typePeer revieweden
dc.description.versionpublishedVersionen
dc.identifier.doihttps://doi.org/10.1073/pnas.1720008115
dc.identifier.cristin1600466


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Attribution-NonCommercial 3.0 United States

This is an open access article, originally published at https://doi.org/10.1073/pnas.1720008115
Med mindre annet er angitt, så er denne innførselen lisensiert som Attribution-NonCommercial 3.0 United States This is an open access article, originally published at https://doi.org/10.1073/pnas.1720008115