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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
165
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4329-37
pubmed:dateRevised
2006-11-15
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
pubmed:year
2000
pubmed:articleTitle
IL-15 and IL-15 receptor selectively regulate differentiation of common mucosal immune system-independent B-1 cells for IgA responses.
pubmed:affiliation
Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't