Abstract
C57BL/6 mice are protected from a lethal pneumonia caused by Sendai virus when treated with low doses of mAb directed to the CD3 Ag. The protective mechanism is not due to an accelerated Sendai virus-specific Th cell, CTL, or antibody response but to a strong NK cell response via the in vivo induction of lymphokines. Antibodies directed against the NK1.1 and asialo GM1 marker totally reversed the protective effect of anti-CD3 treatment. In vivo treatment with rIL-2 also induced NK activity and induced antiviral protection. Treatment with anti-CD3 protects when given in a narrow time window (1 day before until 1 day after Sendai virus inoculation), indicating that NK activity is protective in the early phase of virus infection.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antibodies, Monoclonal / therapeutic use*
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Antibodies, Viral / biosynthesis
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Antigens, Differentiation, T-Lymphocyte / physiology*
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CD3 Complex
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Cytotoxicity, Immunologic
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Immunity, Cellular
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Immunotherapy
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Interleukin-2 / biosynthesis
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Interleukin-2 / therapeutic use
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Killer Cells, Natural / immunology*
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Lymphocyte Activation
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Mice
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Mice, Inbred Strains
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Parainfluenza Virus 1, Human
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Paramyxoviridae Infections / therapy*
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Receptors, Antigen, T-Cell / physiology*
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Survival Analysis
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T-Lymphocytes, Cytotoxic / immunology
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Time Factors
Substances
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Antibodies, Monoclonal
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Antibodies, Viral
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Antigens, Differentiation, T-Lymphocyte
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CD3 Complex
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Interleukin-2
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Receptors, Antigen, T-Cell