The JI Acurri Cytometers
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     
 


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Pobezinskaya, Y.
Right arrow Articles by Golovkina, T. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pobezinskaya, Y.
Right arrow Articles by Golovkina, T. V.
The Journal of Immunology, 2004, 172: 5582-5587.
Copyright © 2004 by The American Association of Immunologists

Initial Stages of Mammary Tumor Virus Infection Are Superantigen Independent1

Yelena Pobezinskaya, Alexander V. Chervonsky and Tatyana V. Golovkina2

The Jackson Laboratory, Bar Harbor, ME 04609

Exogenous mouse mammary tumor virus (MMTV) is transmitted via the milk from infected mothers to newborn pups. Efficient MMTV transmission is dependent on proliferation of T cells with particular TCR {beta}-chains, which occurs upon recognition of virally encoded superantigen (SAg) bound to MHC class II molecules. It is assumed that infection of these dividing cells favors MMTV amplification. SAg is important for MMTV infection, as mice that lack SAg-cognate T cells due to expression of endogenous Mtv loci or mice that express inappropriate MHC haplotypes unable to present viral SAg efficiently were shown to be resistant to MMTV infection. However, this resistance was not absolute, as these mice developed late onset MMTV-induced mammary tumors. In this study, we show that the success of initial MMTV infection in neonates is independent of SAg function but depends on the developmentally regulated proliferation of target cells. However, SAg was absolutely required for virus spread following completion of this proliferative stage.




This article has been cited by other articles:


Home page
J. Virol.Home page
C. M. Okeoma, M. Shen, and S. R. Ross
A Novel Block to Mouse Mammary Tumor Virus Infection of Lymphocytes in B10.BR Mice
J. Virol., February 1, 2008; 82(3): 1314 - 1322.
[Abstract] [Full Text] [PDF]


Home page
J. Virol.Home page
L. K. Case, L. Petell, L. Yurkovetskiy, A. Purdy, K. J. Savage, and T. V. Golovkina
Replication of Beta- and Gammaretroviruses Is Restricted in I/LnJ Mice via the Same Genetic Mechanism
J. Virol., February 1, 2008; 82(3): 1438 - 1447.
[Abstract] [Full Text] [PDF]


Home page
J. Virol.Home page
C. C. MacDearmid, L. K. Case, C. L. Starling, and T. V. Golovkina
Gradual Elimination of Retroviruses in YBR/Ei Mice
J. Virol., March 1, 2006; 80(5): 2206 - 2215.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 2004 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 2004 by The American Association of Immunologists, Inc. All rights reserved.