| pubmed-article:16505356 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16505356 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:16505356 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:16505356 | lifeskim:mentions | umls-concept:C1704410 | lld:lifeskim |
| pubmed-article:16505356 | lifeskim:mentions | umls-concept:C1510827 | lld:lifeskim |
| pubmed-article:16505356 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:16505356 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:16505356 | pubmed:dateCreated | 2006-3-15 | lld:pubmed |
| pubmed-article:16505356 | pubmed:abstractText | Multiple mechanisms of tolerance induction limit autoimmunity, but their relative contribution for lymphocytes recognizing self-antigens of differing availability is incompletely understood. The mechanisms applied to arthritogenic B cells expressing antigen-specific B cell receptors (BCRs) with different affinities for glucose-6-phosphate isomerase (GPI) were examined in the corresponding Ig gene knock-in mice. This ubiquitously expressed and blood-borne enzyme is the target autoantigen in the K/BxN model of inflammatory arthritis and perhaps in some humans with arthritis. Negative selection of B cells expressing high-affinity anti-GPI specificities, whose surface receptors were occupied by GPI, operated mainly at the transitional B cell stages in the spleen, preventing their final differentiation and entry into follicular areas. Receptor editing contributed to the purging of cells displaying anti-GPI BCRs, and significant numbers of autoreactive cells escaped through expression of an additional Ig light (L) chain, accumulating gradually in lymphoid organs. In contrast, low-affinity anti-GPI B cells, whose surface receptors did not carry GPI, matured normally. The "escaped" dual-L-chain cells and the "ignored" low-affinity cells are the likely precursors of cells that produce pathogenic autoantibodies once T cell help is provided. These studies portray, in a single system, the range of tolerance mechanisms applied to potentially pathogenic B cells, and serve as a base for dissecting where T cell help intervenes and where therapeutic agents impinge. | lld:pubmed |
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| pubmed-article:16505356 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16505356 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16505356 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16505356 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16505356 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:16505356 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:16505356 | pubmed:author | pubmed-author:GrusbyMichael... | lld:pubmed |
| pubmed-article:16505356 | pubmed:author | pubmed-author:BenoistChrist... | lld:pubmed |
| pubmed-article:16505356 | pubmed:author | pubmed-author:MathisDianeD | lld:pubmed |
| pubmed-article:16505356 | pubmed:author | pubmed-author:KearneyJohn... | lld:pubmed |
| pubmed-article:16505356 | pubmed:author | pubmed-author:HuangHaochuH | lld:pubmed |
| pubmed-article:16505356 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16505356 | pubmed:day | 7 | lld:pubmed |
| pubmed-article:16505356 | pubmed:volume | 103 | lld:pubmed |
| pubmed-article:16505356 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16505356 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16505356 | pubmed:pagination | 3734-9 | lld:pubmed |
| pubmed-article:16505356 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:16505356 | pubmed:meshHeading | pubmed-meshheading:16505356... | lld:pubmed |
| pubmed-article:16505356 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16505356 | pubmed:articleTitle | Induction of tolerance in arthritogenic B cells with receptors of differing affinity for self-antigen. | lld:pubmed |
| pubmed-article:16505356 | pubmed:affiliation | Section on Immunology and Immunogenetics, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA. | lld:pubmed |
| pubmed-article:16505356 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16505356 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:16505356 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16505356 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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