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Research Article Free access | 10.1172/JCI3248

Apoptosis mediated by Fas but not tumor necrosis factor receptor 1 prevents chronic disease in mice infected with murine cytomegalovirus.

M Fleck, E R Kern, T Zhou, J Podlech, W Wintersberger, C K Edwards 3rd, and J D Mountz

The University of Regensburg, Department of Medicine I, 93042 Regensburg, Germany.

Find articles by Fleck, M. in: PubMed | Google Scholar

The University of Regensburg, Department of Medicine I, 93042 Regensburg, Germany.

Find articles by Kern, E. in: PubMed | Google Scholar

The University of Regensburg, Department of Medicine I, 93042 Regensburg, Germany.

Find articles by Zhou, T. in: PubMed | Google Scholar

The University of Regensburg, Department of Medicine I, 93042 Regensburg, Germany.

Find articles by Podlech, J. in: PubMed | Google Scholar

The University of Regensburg, Department of Medicine I, 93042 Regensburg, Germany.

Find articles by Wintersberger, W. in: PubMed | Google Scholar

The University of Regensburg, Department of Medicine I, 93042 Regensburg, Germany.

Find articles by Edwards, C. in: PubMed | Google Scholar

The University of Regensburg, Department of Medicine I, 93042 Regensburg, Germany.

Find articles by Mountz, J. in: PubMed | Google Scholar

Published October 1, 1998 - More info

Published in Volume 102, Issue 7 on October 1, 1998
J Clin Invest. 1998;102(7):1431–1443. https://doi.org/10.1172/JCI3248.
© 1998 The American Society for Clinical Investigation
Published October 1, 1998 - Version history
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Abstract

The role of Fas- and TNF-receptor 1 (TNF-R1)-mediated apoptosis in the clearance of virally infected cells and in the regulation of the immune response was analyzed after murine cytomegalovirus (MCMV) infection of C57BL/6 (B6)-+/+ mice, Fas-mutant B6-lpr/lpr mice, TNF-R1 knockout B6-tnfr0/0 mice, and double-deficient B6-tnfr0/0 lpr/lpr mice. There was approximately equivalent clearance of MCMV in B6-+/+, B6-tnfr0/0, and B6-lpr/lpr mice, and by day 28 no infectious virus could be detected in the liver, kidney, lung, or peritoneal exudate. However, delayed virus clearance was observed in B6-tnfr0/0 lpr/lpr mice. An acute inflammatory response occurred in the liver, lung, and kidney of all mice, which was most severe 7 d after MCMV infection, but resolved by day 28 in B6-+/+ and B6-tnfr0/0 mice, but not in B6-lpr/lpr or B6-tnfr0/0 lpr/lpr mice. These results indicate that apoptosis mediated by either Fas or TNF-R1 is sufficient for rapid clearance of the virus. However, apoptosis induced by Fas, but not TNF-R1, is required for the downmodulation of the immune response to the virus and prevention of a chronic inflammatory reaction.

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