Linked Life Data

7794824

Source:http://linkedlifedata.com/resource/pubmed/id/7794824

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1995-8-3
pubmed:abstractText
Synovial fluid from patients with rheumatoid arthritis (RA-SF) contains in vivo produced cytokines and inflammatory mediators, including a factor that induces IgG2b production of lipopolysaccharide (LPS) preactivated murine B lymphocytes. In order to determine the mechanism by which RA-SF acts on LPS activated mouse B cells, CBA/N mice were used as an experimental model. The X-linked immunodeficiency of these mice is caused by a point mutation in the Bruton's tyrosine kinase (btk) gene. We have earlier shown that RA-SF can reconstitute the CBA/N B cell deficiency in vitro and in vivo, with regard to IgG2b production after LPS stimulation. Since transforming growth factor (TGF)-beta has been suggested to be a switch factor for IgG2b, we aimed at investigating the role of TGF-beta in our experimental system. We found that TGF-beta could not mimic the effect of RA-SF on CBA spleen cells. A small increase of IgG2b secretion was observed with spleen cells from normal CBA mice, whereas Ig secretion of all isotypes was suppressed in CBA/N spleen cells treated with TGF-beta at any concentration. Neutralizing antibodies against TGF-beta suppressed the response of CBA B cells, whereas the response by CBA/N B cells was enhanced by the same antibody preparation. Here we also show that the abnormal B cell responsiveness to TGF-beta, typical of CBA/N, co-segregates with the btk mutation in male (CBA x CBA/N)F2 spleen cells. This was determined by allele specific PCR recognizing the identified base substitutions of the btk gene, typical of the two strains. We propose that RA-SF contains a factor, separate from TGF-beta, that is involved in the differentiation of IgG2b expressing cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0953-8178
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:geneSymbol
btk
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
459-69
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed-meshheading:7794824-Alleles, pubmed-meshheading:7794824-Animals, pubmed-meshheading:7794824-Arthritis, Rheumatoid, pubmed-meshheading:7794824-B-Lymphocytes, pubmed-meshheading:7794824-Base Sequence, pubmed-meshheading:7794824-Biological Factors, pubmed-meshheading:7794824-DNA Mutational Analysis, pubmed-meshheading:7794824-Female, pubmed-meshheading:7794824-Immunoglobulin G, pubmed-meshheading:7794824-Immunologic Deficiency Syndromes, pubmed-meshheading:7794824-Interleukin-4, pubmed-meshheading:7794824-Lipopolysaccharides, pubmed-meshheading:7794824-Lymphocyte Activation, pubmed-meshheading:7794824-Male, pubmed-meshheading:7794824-Mice, pubmed-meshheading:7794824-Mice, Inbred CBA, pubmed-meshheading:7794824-Mice, Mutant Strains, pubmed-meshheading:7794824-Molecular Sequence Data, pubmed-meshheading:7794824-Point Mutation, pubmed-meshheading:7794824-Polymerase Chain Reaction, pubmed-meshheading:7794824-Protein-Tyrosine Kinases, pubmed-meshheading:7794824-Synovial Fluid, pubmed-meshheading:7794824-Transforming Growth Factor beta, pubmed-meshheading:7794824-X Chromosome
pubmed:year
1995
pubmed:articleTitle
Differential sensitivity to transforming growth factor (TGF)-beta of CBA and of CBA/N B cells demonstrates that the IgG2b inducing factor in synovial fluid from rheumatoid arthritis patients is not identical to TGF-beta.
pubmed:affiliation
Department of Immunology, Arrhénius Laboratories for Natural Sciences, Stockholm University, Sweden.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't