In:
Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 96, No. 9 ( 1999-04-27), p. 5135-5140
Abstract:
The lack of B cells and antibody does not prevent mice from dealing effectively with a pathogenic γ-herpesvirus. Both CD4 + and CD8 + T cells contribute to the control of virus replication in the respiratory tract, with the depletion of either lymphocyte subset leading to increased titers in the lung. However, the further neutralization of IFN-γ diminishes the effectiveness of the CD4 + T cell response and causes substantially increased mortality. Experiments with bone marrow radiation chimeras indicate that the immune CD4 + effectors operate optimally when there is the potential for direct interaction with virus-infected targets expressing MHC class II glycoproteins, suggesting that the IFN-γ produced by these lymphocytes is functioning at short range. The numbers of latently infected cells in the spleens of carrier mice are also significantly increased by the concurrent depletion of both the CD4 + population and IFN-γ. These experiments raise the possibility that the defective control of intercurrent γ-herpesvirus infections in patients with AIDS not only is due solely to the absence of helper T cells but also reflects the loss of an important set of CD4 + effectors.
Type of Medium:
Online Resource
ISSN:
0027-8424
,
1091-6490
DOI:
10.1073/pnas.96.9.5135
Language:
English
Publisher:
Proceedings of the National Academy of Sciences
Publication Date:
1999
detail.hit.zdb_id:
209104-5
detail.hit.zdb_id:
1461794-8
SSG:
11
SSG:
12
Permalink
