Linked Life Data

17163453

Source:http://linkedlifedata.com/resource/pubmed/id/17163453

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-12-27
pubmed:abstractText
Germ-line (GL) alpha transcription can be induced in mouse splenic B cells by LPS and TGF-beta. This stimulation results in approximately 1% IgA+ cells, which can be increased by IL-4, IL-5, and anti-IgD dextran (alpha delta Dex). To determine the mechanism of this increase, we asked whether IgA class switching correlates with acetylation of histone 3 at S alpha, the switch region for IgA. In the presence of the survival factor B lymphocyte stimulator (BLyS), acetylated histone 3 (AcH3) at S alpha was changed little by TGF-beta in LPS-stimulated mouse splenic B cell cultures, despite induction of GL alpha RNA. Compared with BLyS/LPS/TGF-beta alone, treatment with BLyS/LPS/TGF-beta/IL-4/IL-5/alpha delta Dex increased AcH3 at S alpha fourfold, and also increased GL alpha RNA levels more than eightfold. By contrast, IgG2b class switching was optimal in BLyS/LPS/TGF-beta alone, and was suppressed by IL-4/IL-5/alpha delta Dex. Thus, B cell activators that increase IgA class switching do not increase IgG2b class switching. Further investigation showed that in contrast to purified IgM+ cells, IgG2b+ cells switched poorly to IgA in response to BLyS/LPS/TGF-beta/IL-4/IL-5/ +/- alpha delta Dex. These results suggest that IgA class switching is unusual among isotypes in its requirement for multiple B cell activation signals in addition to LPS and the cytokine that initiates the corresponding GL transcription.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0014-2980
pubmed:author
pubmed:issnType
Print
pubmed:volume
37
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
240-51
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed-meshheading:17163453-Acetylation, pubmed-meshheading:17163453-Animals, pubmed-meshheading:17163453-Antibodies, Anti-Idiotypic, pubmed-meshheading:17163453-B-Cell Activating Factor, pubmed-meshheading:17163453-B-Lymphocytes, pubmed-meshheading:17163453-Cells, Cultured, pubmed-meshheading:17163453-Dextrans, pubmed-meshheading:17163453-Histones, pubmed-meshheading:17163453-Humans, pubmed-meshheading:17163453-Immunoglobulin A, pubmed-meshheading:17163453-Immunoglobulin Class Switching, pubmed-meshheading:17163453-Immunoglobulin G, pubmed-meshheading:17163453-Immunoglobulin Isotypes, pubmed-meshheading:17163453-Interleukin-4, pubmed-meshheading:17163453-Interleukin-5, pubmed-meshheading:17163453-Lymphocyte Activation, pubmed-meshheading:17163453-Mice, pubmed-meshheading:17163453-Mice, Inbred C57BL, pubmed-meshheading:17163453-Spleen, pubmed-meshheading:17163453-Up-Regulation
pubmed:year
2007
pubmed:articleTitle
Stimuli that enhance IgA class switching increase histone 3 acetylation at S alpha, but poorly stimulate sequential switching from IgG2b.
pubmed:affiliation
Immunology and Virology Program, Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, MA 01655, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, N.I.H., Extramural