| First Author | Lucchiari MA | Year | 1992 |
| Journal | Immunobiology | Volume | 185 |
| Issue | 5 | Pages | 475-82 |
| PubMed ID | 1360445 | Mgi Jnum | J:12251 |
| Mgi Id | MGI:60078 | Doi | 10.1016/S0171-2985(11)80089-6 |
| Citation | Lucchiari MA, et al. (1992) In vivo depletion of interferon-gamma leads to susceptibility of A/J mice to mouse hepatitis virus 3 infection. Immunobiology 185(5):475-82 |
| abstractText | The possible role of interferon-gamma (IFN-gamma) in the resistance of A/J mice to MHV3 infection was investigated. Monoclonal antibodies specific for IFN-gamma, CD4 and CD8 molecules were administered in vivo to deplete selectively the IFN-gamma synthesized or the appropriate subset of T cells. The animals were then infected with MHV3 and the course of infection was followed by studying different parameters, such as, the mortality, the virus growth in the tissues and the IFN-gamma synthesis in sera and peritoneal exudates. After MHV3 infection, a full resistance of control A/J mice was observed, in contrast to the high mortality rate observed among the depleted animals, where higher virus titers were found in different tissues. The IFN-gamma synthesis in sera and peritoneal exudates of depleted mice, after MHV3 infection, drastically decreased when compared to that detected in control mice. The data presented are consistent with the hypothesis that IFN-gamma plays an essential role in the resistance of A/J mice to MHV3 infection. |
