rdf:type |
|
lifeskim:mentions |
umls-concept:C0007589,
umls-concept:C0007634,
umls-concept:C0020835,
umls-concept:C0026724,
umls-concept:C0205214,
umls-concept:C0254610,
umls-concept:C0300804,
umls-concept:C0439662,
umls-concept:C0851285,
umls-concept:C0871261,
umls-concept:C1511938,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2911692
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pubmed:issue |
8
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pubmed:dateCreated |
2000-10-24
|
pubmed:abstractText |
We show in this report a new regulatory role for IL-15 and IL-15R in the development of B-1 cells and their differentiation into IgA-producing cells. Mucosal IgA levels were found to be inhibited by anti-IL-15 mAb treatment in vivo, but enhanced by administration of rIL-15, while serum IgA levels remained unaffected. Mucosal B-1 cells preferentially proliferated in response to IL-15 in vitro. When mucosal B-1 and B-2 cells were separated into surface (s)IgM(+)sIgA(-) and sIgM(-)sIgA(+) fractions, IL-15R-specific mRNA was found to be predominant in both sIgM(+)sIgA(-) and sIgM(-)sIgA(+) B-1 cells at a much higher level than B-2 cells. Further, incubation of these different subsets of B-1 and B-2 cells with IL-15 resulted in greater enhancement of the corresponding receptor expression by B-1 subset when compared with B-2 fraction. Interestingly, de novo isolated sIgM(+)sIgA(-) B-1, but not sIgM(+)sIgA(-) B-2, cells were already class-switched cells because the germline Calpha transcript was detected and was then further enhanced by IL-15. IL-15 also supported differentiation of both sIgM(+)sIgA(-) and sIgM(-)sIgA(+) B-1 cells into IgA-producing cells. Taken together, these findings suggest that IL-15 is a critically important cytokine for the differentiation of both sIgM(+),IgA(-) and sIgM(-)sIgA(+) B-1 cells expressing IL-15R into IgA-producing cells in mucosal tissues.
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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/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Il15ra protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin A, Secretory,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin E,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-15,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-15,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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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 |
165
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
4329-37
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11035068-Animals,
pubmed-meshheading:11035068-Antibodies, Monoclonal,
pubmed-meshheading:11035068-B-Lymphocytes,
pubmed-meshheading:11035068-Cell Differentiation,
pubmed-meshheading:11035068-Cells, Cultured,
pubmed-meshheading:11035068-Immunity, Mucosal,
pubmed-meshheading:11035068-Immunoglobulin A, Secretory,
pubmed-meshheading:11035068-Immunoglobulin E,
pubmed-meshheading:11035068-Injections, Intraperitoneal,
pubmed-meshheading:11035068-Interleukin-15,
pubmed-meshheading:11035068-Intestinal Mucosa,
pubmed-meshheading:11035068-Lymphocyte Activation,
pubmed-meshheading:11035068-Mice,
pubmed-meshheading:11035068-Mice, Inbred C57BL,
pubmed-meshheading:11035068-Peritoneal Cavity,
pubmed-meshheading:11035068-Receptors, Interleukin-15,
pubmed-meshheading:11035068-Receptors, Interleukin-2,
pubmed-meshheading:11035068-Spleen,
pubmed-meshheading:11035068-Transcription, Genetic
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pubmed:year |
2000
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pubmed:articleTitle |
IL-15 and IL-15 receptor selectively regulate differentiation of common mucosal immune system-independent B-1 cells for IgA responses.
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pubmed:affiliation |
Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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