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Regulation of natural killer cell activity by anti-I-region monoclonal antibodies
Authors:Somesh D Sharma  Teresa Budzich  Max R Proffitt  Diane Shepherd  Jack S Remington
Institution:1. Department of Immunology and Infectious Diseases, Research Institute, Palo Alto Medical Foundation, 860 Bryant Street, Palo Alto, California 94301 U.S.A.;2. Division of Infectious Diseases, Department of Medicine, Stanford University Medical Center, Stanford, California 94305 U.S.A.;3. Department of Molecular and Cell Biology, Research Division, Cleveland Clinic Foundation, Cleveland, Ohio 44106 U.S.A.
Abstract:The effects of a monoclonal antibody directed against immune response gene products on mouse NK activity were examined. In vivo administration of an anti-I-Ak antibody to C3H/He (H-2k) mice modulated their peritoneal cell (PC) and spleen cell (SC) natural killer (NK) activity against YAC-1 lymphoma target cells in vitro. No such effect was observed when BALB/c (H-2d) mice were treated with this antibody. Administration of anti-I-Ak antibody to mice before and after infection with Toxoplasma or treatment with poly(I:C) leads to suppression of NK activity in comparison to NK activity of mice infected with Toxoplasma or injected with poly(I:C) alone. A similar treatment regimen with M5/114 antibody which reacts with I-Ab, I-Ad, I-Ed, and I-Ek molecules resulted in decreased NK activity in B10.D2 (H-2d) but not in B10.BR (H-2k) mice. Serum and cell culture supernatant interferon (IFN) concentrations were not altered as a result of anti-I-Ak treatment. Removal of adherent cells did not restore NK activity of anti-I-Ak-treated Toxoplasma-infected mice to levels obtained with mice infected with Toxoplasma. In contrast, depletion of Ly 2.1+ cells from nylon-wool nonadherent SC of mice treated with anti-I-Ak antibody, before and after infection with Toxoplasma, resulted in restoration of NK activity to the same level as that observed in Toxoptasma-infected mice.
Keywords:To whom all correspondence should be addressed at the Research Institute  
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