J Gen Virol Email Content Delivery
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
Right arrow Citation Map
Services
Right arrow Email this article to a friend
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
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ohashi, T.
Right arrow Articles by Kannagi, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ohashi, T.
Right arrow Articles by Kannagi, M.
Agricola
Right arrow Articles by Ohashi, T.
Right arrow Articles by Kannagi, M.

Journal of General Virology, Vol 80, 209-216, Copyright © 1999 by Society for General Microbiology


ARTICLES

Role of class I major histocompatibility complex-restricted and - unrestricted suppression of human immunodeficiency virus type 1 replication by CD8+ T lymphocytes

T Ohashi, M Kubo, H Kato, A Iwamoto, H Takahashi, M Fujii and M Kannagi
Department of Immunotherapeutics, Tokyo Medical and Dental University, Japan.

CD8+ T lymphocytes of asymptomatic human immunodeficiency virus type 1 (HIV-1) carriers (ACs) are capable of suppressing HIV-1 replication in CD4+ peripheral blood mononuclear cells (PBMC) by a variety of known and unknown mechanisms. In the present study, cell contact-dependent, major histocompatibility complex type I (MHC I)-unrestricted, CD8+ cell- mediated suppression of HIV-1 LAI replication was detected. CD8+ PBMC of ACs suppressed HIV-1 replication more efficiently in MHC I-matched CD4+ PBMC than in mismatched cells. However, even when MHC I was totally mismatched, CD8+ cells still suppressed replication to a considerable extent in CD4+ PBMC. This MHC I-unrestricted, CD8+ cell- mediated HIV-1 suppression required cell contact and was not effective against cells of the established T cell line ILT-KK. In contrast, MHC I- restricted HIV-1 suppression by CD8+ T cells was detected when ILT-KK cells were used as a target. By using these systems, we examined MHC I- restricted and -unrestricted suppressive activities of CD8+ cells in various donors in more detail. Although both types of CD8+ cell- mediated HIV-1 suppression diminished at the advanced stage of the infection, MHC I-unrestricted suppression diminished earlier than MHC I- restricted suppression, in parallel with the decline in CD4+ T cells. These results suggest that suppression by the MHC I-restricted mechanism alone may fail to protect against CD4+ T-cell loss at the late stage of infection.


This article has been cited by other articles:


Home page
J. Gen. Virol.Home page
M. Kubo, H. Nishitsuji, K. Kurihara, T. Hayashi, T. Masuda, and M. Kannagi
Suppression of human immunodeficiency virus type 1 replication by arginine deiminase of Mycoplasma arginini
J. Gen. Virol., June 1, 2006; 87(6): 1589 - 1593.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 1999 by the Society for General Microbiology.