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Spontaneous B cell hyperactivity in autoimmune-prone MRL mice

Nijnik, Anastasia; Ferry, Helen; Lewis, Graham; Rapsomaniki, Eleni; Leung, Janson C H; Daser, Angelika; Lambe, Teresa; Goodnow, Christopher; Cornall, Richard J

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The MRL-lpr/lpr mouse strain is a commonly used model of the human autoimmune disease systemic lupus erythematosus (SLE). Although much is known about the contribution of the lpr Fas mutation to B cell tolerance breakdown, the role of the genetic background of the MRL strain itself is less well explored. In this study, we use the MD4 anti-hen egg lysozyme Ig (IgHEL) transgenic system to explore B cell function in MRL+/+ and non-autoimmune mice. We demonstrate that MRL IgHEL B cells show...[Show more]

dc.contributor.authorNijnik, Anastasia
dc.contributor.authorFerry, Helen
dc.contributor.authorLewis, Graham
dc.contributor.authorRapsomaniki, Eleni
dc.contributor.authorLeung, Janson C H
dc.contributor.authorDaser, Angelika
dc.contributor.authorLambe, Teresa
dc.contributor.authorGoodnow, Christopher
dc.contributor.authorCornall, Richard J
dc.date.accessioned2015-12-13T22:50:40Z
dc.identifier.issn0953-8178
dc.identifier.urihttp://hdl.handle.net/1885/80892
dc.description.abstractThe MRL-lpr/lpr mouse strain is a commonly used model of the human autoimmune disease systemic lupus erythematosus (SLE). Although much is known about the contribution of the lpr Fas mutation to B cell tolerance breakdown, the role of the genetic background of the MRL strain itself is less well explored. In this study, we use the MD4 anti-hen egg lysozyme Ig (IgHEL) transgenic system to explore B cell function in MRL+/+ and non-autoimmune mice. We demonstrate that MRL IgHEL B cells show spontaneous hyperactivity in the absence of self-antigen, which is associated with low total B cell numbers but an expansion of the marginal zone B cell population. However, B cell anergy is normal in the presence of soluble lysozyme [soluble hen egg lysozyme (sHEL)], and MRL IgHEL B cells undergo normal elimination in the presence of sHEL when competing with a polyclonal C57BL/6 B cell repertoire. We conclude that B cell hyperactivity may contribute to the autoimmune phenotype of MRL+/+ and MRL-lpr/lpr strains when it initiates antibody responses to rare or sequestered antigens that are below the threshold for tolerance induction, but that there is no B cell intrinsic defect in anergy in MRL mice.
dc.publisherOxford University Press
dc.sourceInternational Immunology
dc.subjectKeywords: cell antigen; immunoglobulin; lysozyme; animal cell; animal experiment; animal model; antibody response; article; autoimmune disease; autoimmunity; B lymphocyte; clonal anergy; controlled study; egg; hen; immunological tolerance; immunoreactivity; lymphoc B lymphocytes; Systemic lupus erythematosus (SLE); Tolerance
dc.titleSpontaneous B cell hyperactivity in autoimmune-prone MRL mice
dc.typeJournal article
local.description.notesImported from ARIES
local.description.refereedYes
local.identifier.citationvolume18
dc.date.issued2006
local.identifier.absfor110703 - Autoimmunity
local.identifier.ariespublicationMigratedxPub9193
local.type.statusPublished Version
local.contributor.affiliationNijnik, Anastasia, Oxford University
local.contributor.affiliationFerry, Helen, Oxford University
local.contributor.affiliationLewis, Graham, Oxford University
local.contributor.affiliationRapsomaniki, Eleni, Oxford University
local.contributor.affiliationLeung, Janson C H, Oxford University
local.contributor.affiliationDaser, Angelika, Oxford University
local.contributor.affiliationLambe, Teresa, Oxford University
local.contributor.affiliationGoodnow, Christopher, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationCornall, Richard J, Oxford University
local.description.embargo2037-12-31
local.bibliographicCitation.issue7
local.bibliographicCitation.startpage1127
local.bibliographicCitation.lastpage1137
local.identifier.doi10.1093/intimm/dxl047
dc.date.updated2015-12-11T10:41:48Z
local.identifier.scopusID2-s2.0-33745236701
CollectionsANU Research Publications

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