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rdf:type |
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lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0026809,
umls-concept:C0039194,
umls-concept:C0042769,
umls-concept:C0085358,
umls-concept:C0237753,
umls-concept:C0597404,
umls-concept:C0871261,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1704243,
umls-concept:C1704632,
umls-concept:C1706438,
umls-concept:C1706817,
umls-concept:C2698600,
umls-concept:C2911692
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pubmed:issue |
1
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pubmed:dateCreated |
1994-10-20
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pubmed:abstractText |
Antibody production profiles have been compared for Sendai virus infection of normal mice and mice that lack CD8+ T cells as a consequence of treatment with a lymphocyte subset-specific monoclonal antibody or homozygous disruption of the beta 2-microglobulin (beta 2-m(-/-)) gene encoding the light chain of the class I major histocompatibility complex glycoprotein. Using the single-cell ELISPOT assay, we show a relative increase in IgA antibody forming cell (AFC) numbers in the mediastinal lymph node (MLN), spleen, and bone marrow of the CD8-depleted mice. This is reflected in higher serum IgA titers. Similarly, secondary infection with a large dose of Sendai virus leads to greater prevalence of virus-specific IgA AFCs as early as Day 5 postinfection in the beta 2-m(-/-) mice. Also, in primed beta 2-m(-/-) mice challenged with vaccinia constructs containing the genes for the hemagglutinin-neuraminidase (HN), nuclear protein, or the fusion protein of Sendai virus, the majority of the virus-specific AFCs in the MLN are specific for HN and secrete IgA.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0042-6822
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
204
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
234-41
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8091654-Animals,
pubmed-meshheading:8091654-Antibodies, Monoclonal,
pubmed-meshheading:8091654-Antibodies, Viral,
pubmed-meshheading:8091654-Antigens, CD8,
pubmed-meshheading:8091654-B-Lymphocytes,
pubmed-meshheading:8091654-Bone Marrow,
pubmed-meshheading:8091654-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:8091654-Female,
pubmed-meshheading:8091654-Immunoglobulin A,
pubmed-meshheading:8091654-Immunoglobulin Isotypes,
pubmed-meshheading:8091654-Lymph Nodes,
pubmed-meshheading:8091654-Lymphocyte Depletion,
pubmed-meshheading:8091654-Mice,
pubmed-meshheading:8091654-Mice, Inbred C57BL,
pubmed-meshheading:8091654-Mice, Transgenic,
pubmed-meshheading:8091654-Parainfluenza Virus 1, Human,
pubmed-meshheading:8091654-Paramyxoviridae Infections,
pubmed-meshheading:8091654-Spleen,
pubmed-meshheading:8091654-T-Lymphocytes,
pubmed-meshheading:8091654-Vaccinia virus,
pubmed-meshheading:8091654-beta 2-Microglobulin
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pubmed:year |
1994
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pubmed:articleTitle |
Mice lacking CD8+ T cells develop greater numbers of IgA-producing cells in response to a respiratory virus infection.
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pubmed:affiliation |
Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38101.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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