Linked Life Data

2959722

Source:http://linkedlifedata.com/resource/pubmed/id/2959722

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1987-11-25
pubmed:abstractText
In previous studies we demonstrated that BALB/c mice bearing ascitic tumors of the IgE-secreting hybridoma B53 (epsilon, kappa, anti-dinitrophenyl) developed large numbers of Lyt-1-2+ Fc epsilon R(+) T lymphocytes (T cells with membrane Fc receptors) in response to the elevated serum IgE concentration. The development of Fc epsilon R(+) T lymphocytes was followed by a progressive decrease in the levels of serum IgE in spite of continued proliferation of the hybridoma cells. This sequence of events suggested that the IgE-secreting hybridoma triggered a suppressive immunoregulatory circuit of the host that inhibited IgE expression by the hybridoma cells. The present studies were undertaken to investigate the basis for the subsequent decline in serum IgE levels in mice with B53 tumors and to identify host factors that might be involved in this process. We observed that ascitic B53 cells recovered at increasing time points from BALB/c mice exhibited a selective decline in steady state levels and rates of synthesis of epsilon-heavy chain protein and mRNA. The expression of kappa-light chain protein and mRNA appeared relatively unchanged. The decrease in epsilon-heavy chain gene expression did not occur when B53 tumors were passaged in nu+/nu+ mice or in BALB/c mice depleted of Lyt-2+ cells (suppressor/cytotoxic cell lineage), but did occur in nu+/nu+ mice reconstituted with neonatal BALB/c thymus and in BALB/c mice depleted of L3T4+ cells (helper/inducer cell lineage). That Fc epsilon R(+) T lymphocytes were directly involved in the inhibition of IgE expression was supported by the earlier and more pronounced inhibition of B53 IgE in mice infused with Fc epsilon R(+) T lymphocytes. We conclude from these findings that: 1) the decline in serum IgE levels that occurs toward the end of each generation of in vivo passage of the B53 hybridoma is due to decreased production of IgE by the hybridoma cells, 2) the decreased production of IgE is due to a selective loss of epsilon mRNA expression, 3) the decrease production of IgE by B53 cells is dependent on the presence of Lyt-2+ cells, and 4) Fc epsilon R(+) T lymphocytes participate in the mechanism by which IgE production is suppressed.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
139
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2865-72
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:2959722-Animals, pubmed-meshheading:2959722-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:2959722-Antigens, Ly, pubmed-meshheading:2959722-Cytoplasm, pubmed-meshheading:2959722-Dinitrobenzenes, pubmed-meshheading:2959722-Gene Expression Regulation, pubmed-meshheading:2959722-Hybridomas, pubmed-meshheading:2959722-Immunoglobulin E, pubmed-meshheading:2959722-Immunoglobulin epsilon-Chains, pubmed-meshheading:2959722-Immunoglobulin kappa-Chains, pubmed-meshheading:2959722-Mice, pubmed-meshheading:2959722-Mice, Nude, pubmed-meshheading:2959722-RNA, Messenger, pubmed-meshheading:2959722-Receptors, Fc, pubmed-meshheading:2959722-Receptors, IgE, pubmed-meshheading:2959722-T-Lymphocytes, pubmed-meshheading:2959722-Thymus Gland, pubmed-meshheading:2959722-Transcription, Genetic
pubmed:year
1987
pubmed:articleTitle
Thymus-dependent in vivo suppression of IgE synthesis in a murine IgE-secreting hybridoma.
pubmed:affiliation
Department of Pathology, University of Iowa College of Medicine, Iowa City 52242.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't