Role of NK cells in immunomodulator-mediated resistance to herpesvirus infection.
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| Abstract |
Seven chemically diverse biological response modifiers (BRM) were compared for antiviral activity in intact and NK cell-depleted CD-1 mice. Both spontaneous and BRM-induced splenic NK cell cytotoxicity were depleted for at least 5 days following treatment with the monoclonal antibody NK1.1. Antiviral protection of standard doses of MVE-2, pIC, pICLC, rmIFN-tau and CL246,738 against lethal MCMV or HSV-2 infections was not abrogated by NK cell depletion, demonstrating that NK cells are not required for BRM-induced antiviral activity against these herpesviruses. When mice were treated with 100,000 U of rHuIFN-alpha B/D, NK cells were not required for activity against MCMV, while at a dose of 25,000 U, NK cells appeared to be partially required against MCMV. At lower doses, the activity of rHuIFN-alpha B/D against MCMV appeared dependent upon the presence of NK cells. A similar dose-related requirement for NK cells was observed for activity of OK-432. Thus, at higher doses of rHuIFN-alpha B/D and OK-432, elements of the natural immune system in addition to or other than NK cells are apparently involved, while at lower doses NK cells appear to play a more important role in antiviral protection against MCMV infection.
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| Authors | S C Kunder, L Wu, P S Morahan |
| Journal | Antiviral research (Antiviral Res) Vol. 21 Issue 2 Pg. 103-18 (Jun 1993) ISSN: 0166-3542 [Print] Netherlands |
| PMID | 8393316 (Publication Type: Comparative Study, Journal Article, Research Support, U.S. Gov't, P.H.S.) |
| Chemical References |
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