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. 1997 Nov 3;186(9):1591-6.
doi: 10.1084/jem.186.9.1591.

Antiviral activity of tumor necrosis factor (TNF) is mediated via p55 and p75 TNF receptors (VSports app下载)

J Ruby  1 , H Bluethmann, J J Peschon
Affiliations

Antiviral activity of tumor necrosis factor (TNF) is mediated via p55 and p75 TNF receptors

J Ruby et al. J Exp Med. .

Abstract

The antiviral nature of tumor necrosis factor (TNF) is generally well accepted. TNF appears to induce multiple antiviral mechanisms, and to synergize with interferon (IFN)-gamma in promoting antiviral activities. We infected TNF receptor (TNFR)-deficient mice with the virulent murine pathogen, ectromelia virus (EV), and observed that otherwise resistant mice were susceptible to lethal infection. To study the molecular basis of the antiviral action of TNF, mice were infected with a recombinant vaccinia virus encoding murine TNF (VV-HA-TNF) VSports手机版. In normal mice, the replication of VV-HA-TNF was highly attenuated. In contrast, mice in which the TNFR type 1 (p55) or the TNFR type 2 (p75) were genetically disrupted showed a moderate defect in their capacity to clear the TNF-encoding virus. The contribution of both TNF receptors to the control of VV-HA-TNF was confirmed by the enhanced replication of VV-HA-TNF in mice deficient for both p55 and p75. These observations were corroborated by infecting TNFR-deficient mice with EV. For both infections, the p55 and p75 TNFRs were necessary to maintain normal levels of resistance. Thus, the antiviral activity of TNF is mediated via both TNFRs in vivo. Furthermore, these studies establish that TNF is an important component of the host response to a natural virus infection. .

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Figure 1
Figure 1
Replication of VV-HA-TNF in TNFR mutant mice. Groups of five female mice of the strains indicated were infected intravenously with 107 PFU of VV-HA-TNF. The virus was recovered from the ovaries of mice 3 d after infection. Data represent the mean titer ± SEM for the total ovarian tissue of five individual mice and are representative of four separate experiments. The limit of detection of the plaque-forming assay was 100 PFU and samples below this level were assigned a value of 50 (1.7 log10) PFU. ** P <0.01, compared to wild-type mice, Student's t test. *** P <0.001, compared to wild-type mice.
Figure 2
Figure 2
Replication of EV in TNFR−/− mice. Groups of five male mice of the strains indicated were infected with 5 × 103 PFU of EV (Moscow) in the right hind footpad. The mice were killed 7 d after infection and virus was assayed in the liver, spleen, and inoculated foot. Data are representative of the mean virus titer ± SEM of the tissues shown for five individual mice. For the liver, titers are expressed per gram of tissue. Virus was recovered from the entire spleen and foot. Morbidity of these mice is discussed in the text. Similar data were obtained in a duplicate experiment in which mice were infected with 104 PFU of EV (data not shown). The limit of detection of the plaque-forming assay was 100 PFU and samples below this level were assigned a value of 50 (1.7 log10) PFU. * P <0.05, in comparison with wild-type mice, Student's t test. ** P <0.01, in comparison with wild-type mice. *** P <0.001, in comparison with wild-type mice.
Figure 3
Figure 3
Survival of TNFR−/− mice infected with EV. Groups of five male mice of various strains were infected with 5 × 103 PFU EV in a volume of 20 μl via the footpad. The strains of mice infected were C57BL/6 × 129 (wild-type control, ⋄; p55−/−, □; p75−/−, ○; and p55−/−p75−/−, ▵). Similar observations were made in a duplicate experiment. Morbidity is discussed in the text.
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