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Article: Induction of broadly reactive influenza antibodies increases susceptibility to autoimmunity

TitleInduction of broadly reactive influenza antibodies increases susceptibility to autoimmunity
Authors
Keywordsantibody
autoimmunity
influenza
universal influenza vaccine
Issue Date2022
Citation
Cell reports, 2022, v. 38, n. 10, p. 110482 How to Cite?
AbstractInfection and vaccination repeatedly expose individuals to antigens that are conserved between influenza virus subtypes. Nevertheless, antibodies recognizing variable influenza epitopes greatly outnumber antibodies reactive against conserved epitopes. Elucidating factors contributing to the paucity of broadly reactive influenza antibodies remains a major obstacle for developing a universal influenza vaccine. Here, we report that inducing broadly reactive influenza antibodies increases autoreactive antibodies in humans and mice and exacerbates disease in four distinct models of autoimmune disease. Importantly, transferring broadly reactive influenza antibodies augments disease in the presence of inflammation or autoimmune susceptibility. Further, broadly reactive influenza antibodies spontaneously arise in mice with defects in B cell tolerance. Together, these data suggest that self-tolerance mechanisms limit the prevalence of broadly reactive influenza antibodies, which can exacerbate disease in the context of additional risk factors.
Persistent Identifierhttp://hdl.handle.net/10722/311982
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLabombarde, Jocelyn G.-
dc.contributor.authorPillai, Meenu R.-
dc.contributor.authorWehenkel, Marie-
dc.contributor.authorLin, Chun Yang-
dc.contributor.authorKeating, Rachael-
dc.contributor.authorBrown, Scott A.-
dc.contributor.authorCrawford, Jeremy Chase-
dc.contributor.authorBrice, David C.-
dc.contributor.authorCastellaw, Ashley H.-
dc.contributor.authorMandarano, Alexandra H.-
dc.contributor.authorGuy, Clifford S.-
dc.contributor.authorMejia, Juan R.-
dc.contributor.authorLewis, Carlessia D.-
dc.contributor.authorChang, Ti Cheng-
dc.contributor.authorOshansky, Christine M.-
dc.contributor.authorWong, Sook San-
dc.contributor.authorWebby, Richard J.-
dc.contributor.authorYan, Mei-
dc.contributor.authorLi, Quan Zhen-
dc.contributor.authorMarion, Tony N.-
dc.contributor.authorThomas, Paul G.-
dc.contributor.authorMcGargill, Maureen A.-
dc.date.accessioned2022-04-06T04:31:54Z-
dc.date.available2022-04-06T04:31:54Z-
dc.date.issued2022-
dc.identifier.citationCell reports, 2022, v. 38, n. 10, p. 110482-
dc.identifier.urihttp://hdl.handle.net/10722/311982-
dc.description.abstractInfection and vaccination repeatedly expose individuals to antigens that are conserved between influenza virus subtypes. Nevertheless, antibodies recognizing variable influenza epitopes greatly outnumber antibodies reactive against conserved epitopes. Elucidating factors contributing to the paucity of broadly reactive influenza antibodies remains a major obstacle for developing a universal influenza vaccine. Here, we report that inducing broadly reactive influenza antibodies increases autoreactive antibodies in humans and mice and exacerbates disease in four distinct models of autoimmune disease. Importantly, transferring broadly reactive influenza antibodies augments disease in the presence of inflammation or autoimmune susceptibility. Further, broadly reactive influenza antibodies spontaneously arise in mice with defects in B cell tolerance. Together, these data suggest that self-tolerance mechanisms limit the prevalence of broadly reactive influenza antibodies, which can exacerbate disease in the context of additional risk factors.-
dc.languageeng-
dc.relation.ispartofCell reports-
dc.subjectantibody-
dc.subjectautoimmunity-
dc.subjectinfluenza-
dc.subjectuniversal influenza vaccine-
dc.titleInduction of broadly reactive influenza antibodies increases susceptibility to autoimmunity-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.celrep.2022.110482-
dc.identifier.pmid35263574-
dc.identifier.scopuseid_2-s2.0-85126171656-
dc.identifier.volume38-
dc.identifier.issue10-
dc.identifier.spage110482-
dc.identifier.epage-
dc.identifier.eissn2211-1247-
dc.identifier.isiWOS:000768352300004-

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