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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
1998-8-12
|
| pubmed:abstractText |
Recent reports have shown that B cells play a key role in the pathogenesis of T cell-mediated autoimmune diseases such as insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic mice (NOD). We have investigated the role of B lymphocytes as APCs in the generation of autoreactive T cell responses by comparing spontaneous responses to self Ags in B cell-deficient and wild-type NOD mice. We determined that B cell-deficient mice had no spontaneous responses to 65-kDa glutamate decarboxylase (GAD65), its immunodominant peptides, and the 60-kDa heat shock protein. In contrast, these Ags are able to induce proliferative responses in the splenocyte cultures of B cell-positive NOD mice. However, T cells from B-deficient mice conserved the ability to respond to nonself Ags and mitogens. The Ag-presenting function of B cells was pivotal in the autoimmune response, since the proliferation of wild-type splenocytes to GAD65 was completely inhibited by blocking the surface Ig-mediated capture of the protein Ag by B cells. Responses to immunodominant GAD65 peptides were also absent in B cell-deficient NOD mice, suggesting that B cells are crucial with regard to the diversification of the autoimmune response to various self epitopes. We believe our results represent strong evidence that B cells are required as APCs to generate pathogenic autoimmune T cell responses and provide a direct correlation between the protection from autoimmune diabetes previously reported in B cell-deficient NOD mice and the lack of anti-GAD65 and anti-heat shock protein 60 T cell responses in these mice.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Blocking,
http://linkedlifedata.com/resource/pubmed/chemical/Autoantigens,
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamate Decarboxylase,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, B-Cell
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
161
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1163-8
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:9686575-Animals,
pubmed-meshheading:9686575-Antibodies, Blocking,
pubmed-meshheading:9686575-Antigen-Presenting Cells,
pubmed-meshheading:9686575-Autoantigens,
pubmed-meshheading:9686575-B-Lymphocytes,
pubmed-meshheading:9686575-Diabetes Mellitus, Type 1,
pubmed-meshheading:9686575-Epitopes,
pubmed-meshheading:9686575-Glutamate Decarboxylase,
pubmed-meshheading:9686575-Immunity, Cellular,
pubmed-meshheading:9686575-Islets of Langerhans,
pubmed-meshheading:9686575-Lymphocyte Activation,
pubmed-meshheading:9686575-Lymphocyte Depletion,
pubmed-meshheading:9686575-Mice,
pubmed-meshheading:9686575-Mice, Inbred NOD,
pubmed-meshheading:9686575-Mice, Knockout,
pubmed-meshheading:9686575-Peptide Fragments,
pubmed-meshheading:9686575-Receptors, Antigen, B-Cell,
pubmed-meshheading:9686575-T-Lymphocyte Subsets
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
B lymphocytes are crucial antigen-presenting cells in the pathogenic autoimmune response to GAD65 antigen in nonobese diabetic mice.
|
| pubmed:affiliation |
Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|