Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-6-22
pubmed:abstractText
Several questions exist regarding CD5+ B cells. These include the ability of these cells, as compared to CD5- B cells, to undergo an Ig isotype class switch, the subclasses utilized, and the effects that switching may have on antigen binding. To address these issues, ten patients with chronic lymphocytic leukemia (CLL) whose CD5+ leukemic B cell clones produced IgG were studied. Monoclonal IgG was collected from PMA-stimulated CLL cells and from heterohybridomas constructed with these cells, and then analyzed for IgG subclass utilization, autoreactivity, and DNA idiotype expression. The monoclonal B cells from 80% of the CLL patients produced IgG1 and those from 20% produced IgG3. None produced IgG2. In contrast to the known autoreactivity of IgM-producing CD5+ CLL cells (> 50% autoreactive), none of these IgG antibodies reacted significantly with the autoantigens tested. However, three did react significantly with autoantigen after artificially increasing antibody valency by crosslinking. Whereas five of the IgG molecules expressed a cross reactive idiotypic (CRI) marker characteristic of non-mutated kappa anti-DNA antibodies, three expressed a CRI displayed primarily on mutated IgG anti-DNA antibodies. Thus, some CD5+ human B cells can undergo an isotype class switch that for these CLL cells is biased against IgG2 and in favor of the IgG1 and IgG3. In their native state the IgG molecules secreted by these isotype-switched CD5+ cells have diminished autoreactivity, as compared to IgM-producing CLL cells. Since some of the IgG antibodies could be made auto- and poly-reactive by increasing antigen-binding valency, while others expressed idiotypic markers of mutated antibodies, certain of these CD5+ B cells probably utilize non-mutated Ig V genes coding for polyreactive antibodies, whereas others may use genes that have undergone somatic mutation and that code for more restricted specificities. Therefore, both valency and VH gene mutation may account for the diminished autoreactivity of these CD5+ B cell-derived IgG antibodies.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0891-6934
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
N
pubmed:pagination
39-48
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:7538331-Adult, pubmed-meshheading:7538331-Aged, pubmed-meshheading:7538331-Animals, pubmed-meshheading:7538331-Antibodies, Antinuclear, pubmed-meshheading:7538331-Antibodies, Neoplasm, pubmed-meshheading:7538331-Antibody Affinity, pubmed-meshheading:7538331-Antibody Specificity, pubmed-meshheading:7538331-Antigens, CD, pubmed-meshheading:7538331-Antigens, CD5, pubmed-meshheading:7538331-Autoimmunity, pubmed-meshheading:7538331-B-Lymphocytes, pubmed-meshheading:7538331-Base Sequence, pubmed-meshheading:7538331-Female, pubmed-meshheading:7538331-Gene Expression Regulation, Neoplastic, pubmed-meshheading:7538331-Gene Rearrangement, B-Lymphocyte, pubmed-meshheading:7538331-Genes, Immunoglobulin, pubmed-meshheading:7538331-Humans, pubmed-meshheading:7538331-Hybridomas, pubmed-meshheading:7538331-Immunoglobulin Class Switching, pubmed-meshheading:7538331-Immunoglobulin G, pubmed-meshheading:7538331-Immunoglobulin Idiotypes, pubmed-meshheading:7538331-Immunoglobulin M, pubmed-meshheading:7538331-Leukemia, Lymphocytic, Chronic, B-Cell, pubmed-meshheading:7538331-Male, pubmed-meshheading:7538331-Mice, pubmed-meshheading:7538331-Middle Aged, pubmed-meshheading:7538331-Molecular Sequence Data, pubmed-meshheading:7538331-Neoplastic Stem Cells, pubmed-meshheading:7538331-Receptors, Antigen, B-Cell
pubmed:year
1994
pubmed:articleTitle
IgG+, CD5+ human chronic lymphocytic leukemia B cells. Production of IgG antibodies that exhibit diminished autoreactivity and IgG subclass skewing.
pubmed:affiliation
Department of Medicine North Shore University Hospital, Manhasset, New York 11030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't