15902303

Source:http://linkedlifedata.com/resource/pubmed/id/15902303

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Predicate	Object
rdf:type	pubmed:Citation
lifeskim:mentions	umls-concept:C0003241, umls-concept:C0004561, umls-concept:C0023434, umls-concept:C0026882, umls-concept:C1709634
pubmed:issue	6
pubmed:dateCreated	2005-6-2
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.
pubmed:grant	http://linkedlifedata.com/resource/pubmed/grant/M01 RR018535, http://linkedlifedata.com/resource/pubmed/grant/R01 CA 81554, http://linkedlifedata.com/resource/pubmed/grant/R01 CA 87956
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pubmed:language	eng
pubmed:journal	http://linkedlifedata.com/resource/pubmed/journal/7802877
pubmed:citationSubset	AIM
pubmed:chemical	http://linkedlifedata.com/resource/pubmed/chemical/Autoantibodies, http://linkedlifedata.com/resource/pubmed/chemical/Complementarity Determining Regions, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, B-Cell
pubmed:status	MEDLINE
pubmed:month	Jun
pubmed:issn	0021-9738
pubmed:author	pubmed-author:AlbesianoEmiliaE, pubmed-author:ChiorazziNicholasN, pubmed-author:HervéMaximeM, pubmed-author:MeffreEricE, pubmed-author:MessmerBradley TBT, pubmed-author:MoeMM, pubmed-author:NgYen-ShingYS, pubmed-author:WardemannHeddaH
pubmed:issnType	Print
pubmed:volume	115
pubmed:owner	NLM
pubmed:authorsComplete	Y
pubmed:pagination	1636-43
pubmed:dateRevised	2009-11-18
pubmed:meshHeading	pubmed-meshheading:15902303-Autoantibodies, pubmed-meshheading:15902303-B-Lymphocytes, pubmed-meshheading:15902303-Base Sequence, pubmed-meshheading:15902303-Cell Lineage, pubmed-meshheading:15902303-Cohort Studies, pubmed-meshheading:15902303-Complementarity Determining Regions, pubmed-meshheading:15902303-Female, pubmed-meshheading:15902303-Humans, pubmed-meshheading:15902303-Leukemia, Lymphocytic, Chronic, B-Cell, pubmed-meshheading:15902303-Male, pubmed-meshheading:15902303-Molecular Sequence Data, pubmed-meshheading:15902303-Neoplastic Stem Cells, pubmed-meshheading:15902303-Receptors, Antigen, B-Cell, pubmed-meshheading:15902303-Somatic Hypermutation, Immunoglobulin
pubmed:year	2005
pubmed:articleTitle	Unmutated and mutated chronic lymphocytic leukemias derive from self-reactive B cell precursors despite expressing different antibody reactivity.
pubmed:affiliation	Laboratory of Biochemistry and Molecular Immunology, Hospital for Special Surgery, New York, New York 10021, USA.
pubmed:publicationType	Journal Article, Clinical Trial, Research Support, U.S. Gov't, P.H.S., Randomized Controlled Trial, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural