Abstract
Mice lacking CD4(+) T cells due to a knock-out mutation respond to vaccination with a replication-defective adenoviral recombinant expressing the glycoprotein of rabies virus with a long-lasting virus-neutralizing antibody response. The vaccine-induced B cells secrete antibodies that are mainly of IgG isotypes. The response can be enhanced upon booster immunization, indicating the induction of B cell memory in the absence of CD4(+) T cells. The antibody response is independent of CD8(+) T cells but requires the presence of CD3(+) cells carrying the NK1.1 markers.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenoviridae / genetics
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Animals
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Antibodies, Viral / biosynthesis*
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Antibody Formation
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Antigens / analysis*
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Antigens, Ly
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Antigens, Surface
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Antigens, Viral*
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B-Lymphocytes / immunology
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CD4 Antigens / physiology
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CD4-Positive T-Lymphocytes / physiology*
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Cell Line
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Glycoproteins / genetics
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Glycoproteins / immunology*
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Immunization
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Immunophenotyping
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Lectins, C-Type
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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NK Cell Lectin-Like Receptor Subfamily B
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Proteins / analysis*
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Rabies Vaccines / immunology*
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Rabies virus / immunology*
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Transgenes
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Vaccines, Synthetic / immunology*
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Viral Envelope Proteins / genetics
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Viral Envelope Proteins / immunology*
Substances
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Antibodies, Viral
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Antigens
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Antigens, Ly
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Antigens, Surface
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Antigens, Viral
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CD4 Antigens
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Glycoproteins
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Klrb1c protein, mouse
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Lectins, C-Type
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NK Cell Lectin-Like Receptor Subfamily B
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Proteins
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Rabies Vaccines
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Vaccines, Synthetic
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Viral Envelope Proteins
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glycoprotein G, Rabies virus