| pubmed-article:15902303 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15902303 | lifeskim:mentions | umls-concept:C0023434 | lld:lifeskim |
| pubmed-article:15902303 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:15902303 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:15902303 | lifeskim:mentions | umls-concept:C0003241 | lld:lifeskim |
| pubmed-article:15902303 | lifeskim:mentions | umls-concept:C1709634 | lld:lifeskim |
| pubmed-article:15902303 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:15902303 | pubmed:dateCreated | 2005-6-2 | lld:pubmed |
| pubmed-article:15902303 | pubmed:abstractText | B cell chronic lymphocytic leukemia (CLL) is a disease of expanding monoclonal B cells whose B cell receptor (BCR) mutational status defines 2 subgroups; patients with mutated BCRs have a more favorable prognosis than those with unmutated BCRs. CLL B cells express a restricted BCR repertoire including antibodies with quasi-identical complementarity-determining region 3 (CDR3), which suggests specific antigen recognition. The antigens recognized by CLL antibodies may include autoantigens since about half of CLL B cells produce autoreactive antibodies. However, the distribution of autoreactive antibodies between Ig heavy-chain variable-unmutated (IgV-unmutated) CLL (UM-CLL) and IgV-mutated CLL (M-CLL) is unknown. To determine the role of antibody reactivity and the impact of somatic hypermutation (SHM) on CLL antibody specificity, we cloned and expressed in vitro recombinant antibodies from M- and UM-CLL B cells and tested their reactivity by ELISA. We found that UM-CLL B cells expressed highly polyreactive antibodies whereas most M-CLL B cells did not. When mutated nonautoreactive CLL antibody sequences were reverted in vitro to their germline counterparts, they encoded polyreactive and autoreactive antibodies. We concluded that both UM-CLLs and M-CLLs originate from self-reactive B cell precursors and that SHM plays an important role in the development of the disease by altering original BCR autoreactivity. | lld:pubmed |
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| pubmed-article:15902303 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15902303 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15902303 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:15902303 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15902303 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:15902303 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:15902303 | pubmed:author | pubmed-author:MoeMM | lld:pubmed |
| pubmed-article:15902303 | pubmed:author | pubmed-author:ChiorazziNich... | lld:pubmed |
| pubmed-article:15902303 | pubmed:author | pubmed-author:WardemannHedd... | lld:pubmed |
| pubmed-article:15902303 | pubmed:author | pubmed-author:MeffreEricE | lld:pubmed |
| pubmed-article:15902303 | pubmed:author | pubmed-author:AlbesianoEmil... | lld:pubmed |
| pubmed-article:15902303 | pubmed:author | pubmed-author:MessmerBradle... | lld:pubmed |
| pubmed-article:15902303 | pubmed:author | pubmed-author:HervéMaximeM | lld:pubmed |
| pubmed-article:15902303 | pubmed:author | pubmed-author:NgYen-ShingYS | lld:pubmed |
| pubmed-article:15902303 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15902303 | pubmed:volume | 115 | lld:pubmed |
| pubmed-article:15902303 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15902303 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15902303 | pubmed:pagination | 1636-43 | lld:pubmed |
| pubmed-article:15902303 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:15902303 | pubmed:meshHeading | pubmed-meshheading:15902303... | lld:pubmed |
| pubmed-article:15902303 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15902303 | pubmed:articleTitle | Unmutated and mutated chronic lymphocytic leukemias derive from self-reactive B cell precursors despite expressing different antibody reactivity. | lld:pubmed |
| pubmed-article:15902303 | pubmed:affiliation | Laboratory of Biochemistry and Molecular Immunology, Hospital for Special Surgery, New York, New York 10021, USA. | lld:pubmed |
| pubmed-article:15902303 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15902303 | pubmed:publicationType | Clinical Trial | lld:pubmed |
| pubmed-article:15902303 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15902303 | pubmed:publicationType | Randomized Controlled Trial | lld:pubmed |
| pubmed-article:15902303 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:15902303 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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