|  Help  |  About  |  Contact Us

Publication : Immune response to mouse mammary tumor virus in mice lacking the alpha/beta interferon or the gamma interferon receptor.

First Author  Maillard I Year  1998
Journal  J Virol Volume  72
Issue  4 Pages  2638-46
PubMed ID  9525580 Mgi Jnum  J:46892
Mgi Id  MGI:1202202 Doi  10.1128/jvi.72.4.2638-2646.1998
Citation  Maillard I, et al. (1998) Immune response to mouse mammary tumor virus in mice lacking the alpha/beta interferon or the gamma interferon receptor. J Virol 72(4):2638-46
abstractText  Mouse mammary tumor virus (MMTV) is a retrovirus which induces a strong immune response and a dramatic increase in the number of infected cells through the expression of a superantigen (SAg). Many cytokines are likely to be involved in the interaction between MMTV and the immune system, In particular, alpha/beta interferon (IFN-alpha/ beta) and gamma interferon (IFN-gamma) exert many antiviral and immunomodulatory activities and play a critical role in other viral infections, In this study, we have investigated the importance of interferons during MMTV infection by using mice with a disrupted IFN-alpha/ beta or IFN-gamma receptor gene, We found that the SAg response to MMTV was not modified in IFN-alpha/beta R-o/o and IFN-gamma R-o/o mice, This was true both for the early expansion of B and T cells induced by the SAg and for the deletion of SAg-reactive cells at later stages of the infection, In addition, no increase in the amount of proviral DNA was detected in tissues of IFN-alpha beta R-o/ o and IFN-gamma R-o/o mice, suggesting that interferons are not essential antiviral defense mechanisms during MMTV infection, In contrast, IFN-gamma R-o/o mice had increased amounts of IL-4 mRNA and an altered usage of immunoglobulin isotypes with a reduced frequency of IgG2a- and IgG3-producing cells, This was associated with lower titers of virus-specific antibodies in serum early after infection, although efficient titers were reached later.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

2 Bio Entities

Trail: Publication

0 Expression