Faculty Research 1990 - 1999

Antiviral activity of NK 1.1+ natural killer cells in C57BL/6 scid mice infected with murine cytomegalovirus.

Document Type

Article

Publication Date

1994

Keywords

Cell-Division, Herpesviridae-Infections: im, Isoantigens: im, Killer-Cells-Natural: im, Lymphocyte-Transformation, Lymphocytic-Choriomeningitis: im, Lymphocytic-Choriomeningitis-Virus: de, Male, Mice, Mice-Inbred-C57BL, Mice-SCID, Muromegalovirus: de, Severe-Combined-Immunodeficiency: im, SUPPORT-U-S-GOVT-P-H-S

First Page

239

Last Page

245

JAX Source

Nat Immun 1994 Sep-Oct;13(5):239-45

Grant

AI17672/AI/NIAID, AI30389/AI/NIAID, CA34461/CA/NCI

Abstract

The activation, proliferation, and antiviral effects of natural killer (NK) cells were examined in a newly developed stock of mice, C57BL/6JSz mice homozygous for the severe combined immunodeficiency (scid) mutation. These mice lack functional T and B cells and express the NK 1.1 alloantigen. Such NK 1.1 expression facilitates the analysis of NK cells and their depletion in vivo with a monoclonal anti-NK 1.1 antibody. These mice, therefore, provide an excellent model to examine unambiguously the interactions between viral infections and NK cells in a system devoid of adaptive immune response mechanisms. Here we show that murine cytomegalovirus (MCMV) and lymphocytic choriomeningitis virus (LCMV) infections resulted in profound levels of NK cell activation. NK cells also proliferated greatly in response to LCMV but generally to a lesser degree in response to MCMV. Depletion of the NK cell activity in vivo caused substantial increases in MCMV synthesis and MCMV-induced pathology. These results further support the concept that NK cells are major regulators of MCMV pathogenesis.

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