Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1995-6-22
pubmed:abstractText
Sort-purified resting murine B cells proliferate in response to dextran-conjugated anti-IgD Abs (alpha delta-dex) but fail to secrete significant amounts of Ig even after the addition of IL-1 + IL-2. We show that either IL-3 or granulocyte-macrophage CSF (GM-CSF) stimulates 10- to 50-fold enhancements in IgM secretion by sort-purified B cells treated with alpha delta-dex + IL-1 + IL-2, and that the combined actions of IL-3 and GM-CSF are typically greater than additive. Both IL-3 and GM-CSF act primarily as B cell differentiation factors, although IL-3 induces a modest enhancement in cellular outgrowth. The enhancing effects of IL-3 and GM-CSF require multivalent Ag receptor cross-linkage, mediated by alpha delta-dex, as neither cytokine induces IgM secretion in the presence of unconjugated anti-IgD Abs. Although both alpha delta-dex and IL-1 + IL-2 are required for optimal IL-3- and GM-CSF-mediated IgM secretion, both IL-3 and GM-CSF stimulate a modest IgM secretory response by cells activated with alpha delta-dex alone. In this regard, supernatant from either an activated CD4+ Th1 or Th2 clone potently induces IgM secretion by alpha delta-dex + IL-1 + IL-2-activated B cells and this is due, in large part, to the presence in these supernatants of either IL-3 and/or GM-CSF. Neither IL-3 nor GM-CSF stimulates significant IgM secretion by B cells activated through the CD40 signaling pathway alone, although the combination of CD40 and membrane Ig signaling leads to a strong enhancement of the IL-3 + GM-CSF-mediated IgM synthesis above that obtained with membrane Ig signaling alone. The demonstration that IL-3 and GM-CSF act directly as differentiation factors for B cells activated through their Ag receptor establishes a novel cytokine pathway for induction of humoral immunity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
154
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5842-50
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:7538533-Animals, pubmed-meshheading:7538533-Antigens, CD, pubmed-meshheading:7538533-Antigens, CD40, pubmed-meshheading:7538533-Antigens, Differentiation, B-Lymphocyte, pubmed-meshheading:7538533-B-Lymphocytes, pubmed-meshheading:7538533-Cell Separation, pubmed-meshheading:7538533-Cells, Cultured, pubmed-meshheading:7538533-Culture Media, Conditioned, pubmed-meshheading:7538533-Cytokines, pubmed-meshheading:7538533-Female, pubmed-meshheading:7538533-Granulocyte-Macrophage Colony-Stimulating Factor, pubmed-meshheading:7538533-Immunoglobulin D, pubmed-meshheading:7538533-Immunoglobulin M, pubmed-meshheading:7538533-Immunoglobulins, pubmed-meshheading:7538533-Interleukin-3, pubmed-meshheading:7538533-Mice, pubmed-meshheading:7538533-Mice, Inbred DBA, pubmed-meshheading:7538533-Receptors, Fc, pubmed-meshheading:7538533-Signal Transduction, pubmed-meshheading:7538533-Th1 Cells, pubmed-meshheading:7538533-Th2 Cells
pubmed:year
1995
pubmed:articleTitle
IL-3 and granulocyte-macrophage colony-stimulating factor strongly induce Ig secretion by sort-purified murine B cell activated through the membrane Ig, but not the CD40, signaling pathway.
pubmed:affiliation
Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't