CD8beta knockout mice mount normal anti-viral CD8+ T cell responses--but why?

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Ressource 1Download: serval:BIB_CCCCAD7E1B6C.P001 (1207.52 [Ko])
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Serval ID
serval:BIB_CCCCAD7E1B6C
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
CD8beta knockout mice mount normal anti-viral CD8+ T cell responses--but why?
Journal
International Immunology
Author(s)
Angelov G.S., Guillaume P., Luescher I.F.
ISSN
1460-2377[electronic]
Publication state
Published
Issued date
2009
Volume
21
Number
2
Pages
123-135
Language
english
Abstract
It has been shown previously that CD8beta in vitro increases the range and the sensitivity of antigen recognition and in vivo plays an important role in the thymic selection of CD8+ T cells. Consistent with this, we report here that CD8+ T cells from CD8beta knockout (KO) P14 TCR transgenic mice proliferate inefficiently in vitro. In contrast to these findings, we also show that CD8beta KO mice mount normal CD8 primary, secondary and memory responses to acute infection with lymphocytic choriomeningitis virus. Tetramer staining and cytotoxic experiments revealed a predominance of CD8-independent CTL in CD8beta KO mice. The TCR repertoire, especially the one of the TCRalpha chain, was different in CD8beta KO mice as compared with B6 mice. Our results indicate that in the absence of CD8beta, CD8-independent TCRs are preferentially selected, which in vivo effectively compensates for the reduced co-receptor function of CD8alphaalpha.
Keywords
Animals, Antigens, CD8/genetics, Antigens, CD8/immunology, Antigens, Viral/genetics, Antigens, Viral/immunology, Arenaviridae Infections/immunology, CD8-Positive T-Lymphocytes/immunology, CD8-Positive T-Lymphocytes/metabolism, Cell Line, Tumor, Cell Proliferation, Cytotoxicity, Immunologic, Interferon-gamma/secretion, Lymphocyte Activation, Lymphocytic choriomeningitis virus/immunology, Mice, Mice, Inbred C57BL, Mice, Knockout, Transfection
Pubmed
Web of science
Open Access
Yes
Create date
12/10/2009 16:05
Last modification date
25/09/2019 7:10
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