1998年7月
Functional competence of T cells in the absence of glycosylphosphatidylinositol-anchored proteins caused by T cell-specific disruption of the Pig-a gene
European Journal of Immunology
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- 巻
- 28
- 号
- 7
- 開始ページ
- 2159
- 終了ページ
- 2166
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1002/(SICI)1521-4141(199807)28:07<2159::AID-IMMU2159>3.0.CO;2-B
- 出版者・発行元
- WILEY-V C H VERLAG GMBH
T lymphocytes express various glycosylphosphatidylinositol (GPI)-anchored surface proteins, such as Thy-1 and Ly-6A. However, functional contribution of GPI-anchored proteins in T cell activation is as yet poorly understood. Here we report the generation of mutant mice deficient in the expression of GPI-anchored molecules exclusively in their T cells. We established mice carrying three identically oriented lox-P sites within the Pig-a gene, which encodes a component essential for the initial step of GPI anchor biosynthesis. These mice were crossed with mice carrying the Cre recombinase gene driven by the T cell-specific p56(lck) proximal promoter. Offspring carrying both the lox-P-containing Pig-a gene and the Cre transgene exhibited almost complete loss of the surface expression of GPI-anchored molecules on peripheral T cells. Interestingly, those T cells deficient in GPI-anchored molecules were capable of responding to T cell receptor stimulation in vitro and in vivo. These results indicate that T cells lacking the expression of GPI-anchored molecules are functionally competent in exerting TCR-mediated immune responses.
- リンク情報
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- DOI
- https://doi.org/10.1002/(SICI)1521-4141(199807)28:07<2159::AID-IMMU2159>3.0.CO;2-B
- CiNii Articles
- http://ci.nii.ac.jp/naid/10005512139
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/9692885
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000075006400013&DestApp=WOS_CPL
- Scopus
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=0031828709&origin=inward 本文へのリンクあり
- Scopus Citedby
- https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=0031828709&origin=inward
- ID情報
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- DOI : 10.1002/(SICI)1521-4141(199807)28:07<2159::AID-IMMU2159>3.0.CO;2-B
- ISSN : 0014-2980
- CiNii Articles ID : 10005512139
- PubMed ID : 9692885
- SCOPUS ID : 0031828709
- Web of Science ID : WOS:000075006400013