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pubmed-article:16735376pubmed:dateCreated2006-6-23lld:pubmed
pubmed-article:16735376pubmed:abstractTextThe 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.lld:pubmed
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pubmed-article:16735376pubmed:pagination1127-37lld:pubmed
pubmed-article:16735376pubmed:dateRevised2007-8-13lld:pubmed
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pubmed-article:16735376pubmed:year2006lld:pubmed
pubmed-article:16735376pubmed:articleTitleSpontaneous B cell hyperactivity in autoimmune-prone MRL mice.lld:pubmed
pubmed-article:16735376pubmed:affiliationHenry Wellcome Building of Molecular Physiology, Oxford University, Roosevelt Drive, Oxford, OX3 7BN, UK.lld:pubmed
pubmed-article:16735376pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:16735376pubmed:publicationTypeComparative Studylld:pubmed
pubmed-article:16735376pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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