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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
1990-12-12
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pubmed:abstractText |
Previously, we reported that cholera toxin (CT) causes LPS-stimulated membrane (m)IgM+ B cells to undergo increased switch differentiation to IgG- and IgA-producing B cells. In this study we determined whether this effect is specific for one or several of the IgG subclasses and whether B cells exposed to CT respond differently to IL-4, a lymphokine with switching capabilities. In initial studies we found that in LPS-stimulated, mIgM+ B cell cultures, CT eightfold enhanced the formation of IgG1-producing B cells, whereas it only weakly enhanced, one- to twofold, the formation of IgG3-producing B cells. In addition, CT synergistically enhanced the induction of IgG1-producing B cells by IL-4, even at plateau concentrations of IL-4. In contrast, IgM and IgG3 responses were suppressed in the CT plus IL-4-containing cultures as compared to those containing only LPS or LPS and CT. Furthermore, CT plus IL-4 had no enhancing effect on the formation of cells producing IgA; on the contrary, the presence of IL-4 led to a reversal of the stimulatory effect of CT on the IgA response. In further studies, we found that CT affected B cell differentiation at the gene level, before final gene recombination has occurred. Thus, CT together with LPS induced faint but detectable germline gamma 1 RNA transcripts not seen with cells cultured in LPS alone. However, more strikingly, CT enhanced by several-fold expression of germline gamma 1 RNA transcripts in LPS-stimulated B cell cultures containing optimal IgG1-inducing concentrations of IL-4. In addition, despite its weakly positive effect on IgG3 production. CT inhibited expression of germline gamma 3 RNA transcripts in cultures containing LPS and caused a further decrease in such transcripts in cultures containing LPS and IL-4. Finally, we found that CT enhanced the in vivo IgG1 but not the IgG3 or IgM anti-DNP serum antibody response of mice immunized with DNP-LPS. Taken together, these studies suggest that CT more strongly promotes B cell differentiation to IgG1 than to any other IgG subclass in LPS-stimulated cultures. CT acts alone or in synergy with IL-4, early in B cell differentiation to promote IgG1 expression in LPS-stimulated B cell cultures, probably by inducing early steps in the switch to this isotype such as the production of germline gamma 1 RNA transcripts.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cholera Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin A,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/RNA
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
145
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3316-24
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1700007-Animals,
pubmed-meshheading:1700007-Antibody Formation,
pubmed-meshheading:1700007-B-Lymphocytes,
pubmed-meshheading:1700007-Cell Differentiation,
pubmed-meshheading:1700007-Cells, Cultured,
pubmed-meshheading:1700007-Cholera Toxin,
pubmed-meshheading:1700007-Drug Synergism,
pubmed-meshheading:1700007-Immunoglobulin A,
pubmed-meshheading:1700007-Immunoglobulin G,
pubmed-meshheading:1700007-Interleukin-4,
pubmed-meshheading:1700007-Lipopolysaccharides,
pubmed-meshheading:1700007-Mice,
pubmed-meshheading:1700007-Mice, Inbred C57BL,
pubmed-meshheading:1700007-RNA
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pubmed:year |
1990
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pubmed:articleTitle |
Cholera toxin acts synergistically with IL-4 to promote IgG1 switch differentiation.
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pubmed:affiliation |
Department of Medical Microbiology and Immunology, University of Göteborg, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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