pubmed-article:16735376 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16735376 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:16735376 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
pubmed-article:16735376 | lifeskim:mentions | umls-concept:C0424295 | lld:lifeskim |
pubmed-article:16735376 | lifeskim:mentions | umls-concept:C0205359 | lld:lifeskim |
pubmed-article:16735376 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:16735376 | pubmed:dateCreated | 2006-6-23 | lld:pubmed |
pubmed-article:16735376 | pubmed:abstractText | 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 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 |
pubmed-article:16735376 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16735376 | pubmed:language | eng | lld:pubmed |
pubmed-article:16735376 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16735376 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16735376 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16735376 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16735376 | pubmed:month | Jul | lld:pubmed |
pubmed-article:16735376 | pubmed:issn | 0953-8178 | lld:pubmed |
pubmed-article:16735376 | pubmed:author | pubmed-author:LambeTeresaT | lld:pubmed |
pubmed-article:16735376 | pubmed:author | pubmed-author:GoodnowChrist... | lld:pubmed |
pubmed-article:16735376 | pubmed:author | pubmed-author:DaserAngelika... | lld:pubmed |
pubmed-article:16735376 | pubmed:author | pubmed-author:NijnikAnastas... | lld:pubmed |
pubmed-article:16735376 | pubmed:author | pubmed-author:CornallRichar... | lld:pubmed |
pubmed-article:16735376 | pubmed:author | pubmed-author:FerryHelenH | lld:pubmed |
pubmed-article:16735376 | pubmed:author | pubmed-author:LewisGrahamG | lld:pubmed |
pubmed-article:16735376 | pubmed:author | pubmed-author:RapsomanikiEl... | lld:pubmed |
pubmed-article:16735376 | pubmed:author | pubmed-author:LeungJanson... | lld:pubmed |
pubmed-article:16735376 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16735376 | pubmed:volume | 18 | lld:pubmed |
pubmed-article:16735376 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16735376 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16735376 | pubmed:pagination | 1127-37 | lld:pubmed |
pubmed-article:16735376 | pubmed:dateRevised | 2007-8-13 | lld:pubmed |
pubmed-article:16735376 | pubmed:meshHeading | pubmed-meshheading:16735376... | lld:pubmed |
pubmed-article:16735376 | pubmed:meshHeading | pubmed-meshheading:16735376... | lld:pubmed |
pubmed-article:16735376 | pubmed:meshHeading | pubmed-meshheading:16735376... | lld:pubmed |
pubmed-article:16735376 | pubmed:meshHeading | pubmed-meshheading:16735376... | lld:pubmed |
pubmed-article:16735376 | pubmed:meshHeading | pubmed-meshheading:16735376... | lld:pubmed |
pubmed-article:16735376 | pubmed:meshHeading | pubmed-meshheading:16735376... | lld:pubmed |
pubmed-article:16735376 | pubmed:meshHeading | pubmed-meshheading:16735376... | lld:pubmed |
pubmed-article:16735376 | pubmed:meshHeading | pubmed-meshheading:16735376... | lld:pubmed |
pubmed-article:16735376 | pubmed:meshHeading | pubmed-meshheading:16735376... | lld:pubmed |
pubmed-article:16735376 | pubmed:meshHeading | pubmed-meshheading:16735376... | lld:pubmed |
pubmed-article:16735376 | pubmed:meshHeading | pubmed-meshheading:16735376... | lld:pubmed |
pubmed-article:16735376 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16735376 | pubmed:articleTitle | Spontaneous B cell hyperactivity in autoimmune-prone MRL mice. | lld:pubmed |
pubmed-article:16735376 | pubmed:affiliation | Henry Wellcome Building of Molecular Physiology, Oxford University, Roosevelt Drive, Oxford, OX3 7BN, UK. | lld:pubmed |
pubmed-article:16735376 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16735376 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:16735376 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16735376 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16735376 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16735376 | lld:pubmed |