Treatment with monoclonal anti-CD3 antibody protects against lethal Sendai virus infection by induction of natural killer cells
| Autor: | Wm, Kast, Ja, Bluestone, Mh, Heemskerk, Joke Spaargaren, Ac, Voordouw, Jd, Ellenhorn, Cj, Melief |
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Antigens
Differentiation T-Lymphocyte Cytotoxicity Immunologic Immunity Cellular Paramyxoviridae Infections Time Factors CD3 Complex Receptors Antigen T-Cell Antibodies Monoclonal Mice Inbred Strains Antibodies Viral Lymphocyte Activation Survival Analysis Parainfluenza Virus 1 Human Killer Cells Natural Mice Animals Interleukin-2 Immunotherapy T-Lymphocytes Cytotoxic |
| Zdroj: | Europe PubMed Central |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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