Treatment with monoclonal anti-CD3 antibody protects against lethal Sendai virus infection by induction of natural killer cells.
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.
Kast
W M
WM
Division of Immunology, The Netherlands Cancer Institute, Amsterdam.
Bluestone
J A
JA
Heemskerk
M H
MH
Spaargaren
J
J
Voordouw
A C
AC
Ellenhorn
J D
JD
Melief
C J
CJ
D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D000914:Antibodies, Viral / Q000096:biosynthesis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000502:physiology*; D017252:CD3 Complex; D003602:Cytotoxicity, Immunologic; D007111:Immunity, Cellular; D007167:Immunotherapy; D007376:Interleukin-2 / Q000096:biosynthesis / Q000627:therapeutic use; D007694:Killer Cells, Natural / Q000276:immunology*; D008213:Lymphocyte Activation; D051379:Mice; D008815:Mice, Inbred Strains; D010222:Parainfluenza Virus 1, Human; D018184:Paramyxoviridae Infections / Q000628:therapy*; D011948:Receptors, Antigen, T-Cell / Q000502:physiology*; D016019:Survival Analysis; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D013997:Time Factors
D000911:Antibodies, Monoclonal; D000914:Antibodies, Viral; D000945:Antigens, Differentiation, T-Lymphocyte; D017252:CD3 Complex; D007376:Interleukin-2; D011948:Receptors, Antigen, T-Cell