| First Author | Benedict CA | Year | 2001 |
| Journal | Immunity | Volume | 15 |
| Issue | 4 | Pages | 617-26 |
| PubMed ID | 11672543 | Mgi Jnum | J:131141 |
| Mgi Id | MGI:3773008 | Doi | 10.1016/s1074-7613(01)00222-9 |
| Citation | Benedict CA, et al. (2001) Lymphotoxins and cytomegalovirus cooperatively induce interferon-beta, establishing host-virus detente. Immunity 15(4):617-26 |
| abstractText | Tumor necrosis factor (TNF)-related cytokines regulate cell death and survival and provide strong selective pressures for viruses, such as cytomegalovirus (CMV), to evolve counterstrategies in order to persist in immune-competent hosts. Signaling by the lymphotoxin (LT)-beta receptor or TNF receptor-1, but not Fas or TRAIL receptors, inhibits the cytopathicity and replication of human CMV by a nonapoptotic, reversible process that requires nuclear factor kappa B (NF-kappa B)-dependent induction of interferon-beta (IFN-beta). Efficient induction of IFN-beta requires virus infection and LT signaling, demonstrating the need for both host and viral factors in the curtailment of viral replication without cellular elimination. LT alpha-deficient mice and LT beta R-Fc transgenic mice were profoundly susceptible to murine CMV infection. Together, these results reveal an essential and conserved role for LTs in establishing host defense to CMV. |
