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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0004561,
umls-concept:C0007634,
umls-concept:C0010592,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0040100,
umls-concept:C0086418,
umls-concept:C0332324,
umls-concept:C0337611,
umls-concept:C0871261,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C1710082,
umls-concept:C1749467,
umls-concept:C1948023,
umls-concept:C2911692
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pubmed:issue |
8
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pubmed:dateCreated |
1990-5-17
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pubmed:abstractText |
In a Th cell-dependent antibody response, the Th act on B cells partly via a helper activity that is cell contact-dependent and cyclosporine A (CsA)-resistant. This activity seems to be required to induce responsiveness of the B cells toward T cell-derived soluble factors (cytokines) generally believed to be essential for B cell proliferation as well as for Ig secretion. In our study, we have investigated a system in which human B cells are stimulated by mutant EL-4 thymoma cells of mouse origin. It was found that human B cells proliferate and secrete Ig (either 1) in the presence of EL-4 cells plus human T cell supernatant (T-SUP), or 2) in the presence of EL-4 cells alone which have been induced with PMA or IL-1. The first situation conformed to the known synergy between CsA-resistant Th signal and cytokines. However, the B response due to PMA-induced EL-4 cells was special. The PMA-inducible helper activity was CsA-sensitive at the same CsA concentration that inhibited IL-2 secretion of EL-4 cells, but the murine factors in EL-4 supernatant had no effect on human B cells; the helper effect did not occur across a semipermeable membrane. Any contribution of soluble factors from contaminating human T cells was ruled out by adding single human B cells by flow microfluorimetry to cultures with EL-4 cells and PMA. Such B cells generated clonal IgM, IgG, and/or IgA responses. CsA, thus, interfered with some cell contact-mediated signal. However, CsA did not reduce the amount of LFA-1 molecules on EL-4 cells. In conclusion, EL-4 cells can induce proliferation and differentiation of human B cells in a soluble factor-independent manner, via CsA-resistant and CsA-sensitive helper activities. This may represent an alternative pathway of B cell activation.
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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/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclosporins,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphocyte Function-Associated...,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphokines,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Leukocyte-Adhesion,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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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 |
144
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2955-60
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:2139073-Animals,
pubmed-meshheading:2139073-Antigens, Differentiation,
pubmed-meshheading:2139073-B-Lymphocytes,
pubmed-meshheading:2139073-Cell Adhesion,
pubmed-meshheading:2139073-Cell Communication,
pubmed-meshheading:2139073-Cyclosporins,
pubmed-meshheading:2139073-Humans,
pubmed-meshheading:2139073-Lymphocyte Activation,
pubmed-meshheading:2139073-Lymphocyte Cooperation,
pubmed-meshheading:2139073-Lymphocyte Function-Associated Antigen-1,
pubmed-meshheading:2139073-Lymphokines,
pubmed-meshheading:2139073-Mice,
pubmed-meshheading:2139073-Receptors, Leukocyte-Adhesion,
pubmed-meshheading:2139073-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:2139073-Tetradecanoylphorbol Acetate,
pubmed-meshheading:2139073-Tumor Cells, Cultured
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pubmed:year |
1990
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pubmed:articleTitle |
Soluble factor-independent stimulation of human B cell response by mouse thymoma cells. Cyclosporine A-resistant and -sensitive cell contact signals.
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pubmed:affiliation |
Department of Medicine, Hôpital Cantonal Universitaire, Genève, Switzerland.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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