Source:http://linkedlifedata.com/resource/pubmed/id/15067092
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
8
|
| pubmed:dateCreated |
2004-4-6
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| pubmed:abstractText |
One mechanism whereby B cells contribute to type 1 diabetes in nonobese diabetic (NOD) mice is as a subset of APCs that preferentially presents MHC class II-bound pancreatic beta cell Ags to autoreactive CD4 T cells. This results from their ability to use cell surface Ig to specifically capture beta cell Ags. Hence, we postulated a diabetogenic role for defects in the tolerance mechanisms normally blocking the maturation and/or activation of B cells expressing autoreactive Ig receptors. We compared B cell tolerance mechanisms in NOD mice with nonautoimmune strains by using the IgHEL and Ig3-83 transgenic systems, in which the majority of B cells recognize one defined Ag. NOD- and nonautoimmune-prone mice did not differ in ability to delete or receptor edit B cells recognizing membrane-bound self Ags. However, in contrast to the nonautoimmune-prone background, B cells recognizing soluble self Ags in NOD mice did not undergo partial deletion and were also not efficiently anergized. The defective induction of B cell tolerance to soluble autoantigens is most likely responsible for the generation of diabetogenic APC in NOD mice.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Apr
|
| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
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| pubmed:volume |
172
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
5086-94
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:15067092-Animals,
pubmed-meshheading:15067092-Antigen Presentation,
pubmed-meshheading:15067092-Antigen-Presenting Cells,
pubmed-meshheading:15067092-Autoantigens,
pubmed-meshheading:15067092-B-Lymphocyte Subsets,
pubmed-meshheading:15067092-Cell Differentiation,
pubmed-meshheading:15067092-Clonal Anergy,
pubmed-meshheading:15067092-Clonal Deletion,
pubmed-meshheading:15067092-Diabetes Mellitus, Type 1,
pubmed-meshheading:15067092-Female,
pubmed-meshheading:15067092-Membrane Proteins,
pubmed-meshheading:15067092-Mice,
pubmed-meshheading:15067092-Mice, Inbred C57BL,
pubmed-meshheading:15067092-Mice, Inbred NOD,
pubmed-meshheading:15067092-Mice, Transgenic,
pubmed-meshheading:15067092-RNA Editing,
pubmed-meshheading:15067092-Receptors, Antigen, T-Cell,
pubmed-meshheading:15067092-Solubility
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| pubmed:year |
2004
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| pubmed:articleTitle |
B cell selection defects underlie the development of diabetogenic APCs in nonobese diabetic mice.
|
| pubmed:affiliation |
The Jackson Laboratory, Bar Harbor, ME 04609, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|