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Migration inhibition caused by EBV-specific 48K subcomponent of EBNA and the associated 53K cellular protein.

作者信息

Szigeti R, Luka J, Sternås L, Klein G

出版信息

Int J Cancer. 1982 Apr 15;29(4):413-6. doi: 10.1002/ijc.2910290409.

Abstract

Leukocytes from EBV-seropositive but not seronegative healthy donors responded with significant migration inhibition to the 48K subcomponent of the Epstein-Barr virus determined nuclear antigen (EBNA), known to carry the virally determined antigenic specificity. A concentration of 10 micrograms/ml was still effective while 5 micrograms/ml had no detectable effect. EBNA-associated cellular 53K protein had no effect by itself, but it potentiated the effect of 48K, even if the latter was added at the subliminal concentration of 5 micrograms/ml. The related 53K protein, isolated from EBV-negative human lymphoma cells, was also effective, whereas the corresponding murine-tumor-associated 53K had no potentiating effect. Immunization of mice with an extract of DNA-binding proteins from EBV-carrying Raji cells, known to contain both 48K and 53K, induced a significant macrophage migration inhibition response, to both human 48K and 53K. Murine 53K was ineffective, however. Human but not murine 53K increased the migration inhibitory activity of subliminal concentrations of 48K in the murine macrophage system as well. These findings suggest that human but not murine 53K may reconstitute with 48K (EBNA) to form a highly immunogenic complex.

摘要

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