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


     
 

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Wegmann, K. W.
Right arrow Articles by Green, W. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wegmann, K. W.
Right arrow Articles by Green, W. R.

The Journal of Immunology, Vol 149, Issue 5 1593-1598, Copyright © 1992 by American Association of Immunologists

ARTICLES

Generation of anti-AKR/gross murine leukemia virus cytotoxic T lymphocytes (CTL). An analysis of precursor CTL frequencies in the AKR.H-2b and C57BL/6 mouse strains

KW Wegmann, RF Rich and WR Green
Department of Microbiology, Dartmouth Medical School, Lebanon, NH.

C57BL/6 mice, after immunization and secondary in vitro restimulation with AKR/Gross murine leukemia virus (MuLV)-induced tumors, generate AKR/Gross MuLV-specific CTL. After similar immunization protocols, AKR- H-2b mice fail to generate CTL specific for AKR/Gross MuLV. The basis for nonresponsiveness in AKR.H-2b mice is unknown, however, unlike C57BL/6 mice, AKR.H-2b mice carry endogenous proviruses and express N- ecotropic viral Ag. Thus, clonal deletion of pCTL populations due to the expression of AKR/Gross MuLV-like Ag is a likely mechanism for the nonresponsiveness. To determine if nonresponsiveness is due to clonal deletion, limiting dilution cultures were performed to assess the presence of pCTL specific for AKR/Gross MuLV. Our study demonstrates that the frequencies of pCTL specific for AKR/Gross MuLV are similar in both the responder C57BL/6 and nonresponder AKR.H-2b strains. The observation that normal levels of AKR/Gross MuLV-specific pCTL exist in AKR.H-2b mice, suggests that clonal deletion of pCTL is not responsible for the inability of AKR.H-2b mice to generate anti-AKR/Gross virus- specific CTL.


This article has been cited by other articles:


Home page
 J. Immunol.Home page
R. F. Rich and W. R. Green
Characterization of the Fas Ligand/Fas-Dependent Apoptosis of Antiretroviral, Class I MHC Tetramer-Defined, CD8+ CTL by In Vivo Retrovirus-Infected Cells
J. Immunol., March 15, 2002; 168(6): 2751 - 2758.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
R. F. Rich and W. R. Green
Antiretroviral Cytolytic T-Lymphocyte Nonresponsiveness: FasL/Fas-Mediated Inhibition of CD4+ and CD8+ Antiviral T Cells by Viral Antigen-Positive Veto Cells
J. Virol., May 1, 1999; 73(5): 3826 - 3834.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1992 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1992 by The American Association of Immunologists, Inc. All rights reserved.