HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Institute for Genetic Medicine >
Peer-reviewed Journal Articles, etc >

Functional analysis of Foxp3 and CTLA-4 expressing HTLV-1-infected cells in a rat model

Files in This Item:
MI11-12_p964-972.pdf2.54 MBPDFView/Open
Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/39626

Title: Functional analysis of Foxp3 and CTLA-4 expressing HTLV-1-infected cells in a rat model
Authors: Takayanagi, Ryo Browse this author
Ohashi, Takashi Browse this author
Shida, Hisatoshi Browse this author
Keywords: HTLV-1
ATL
Foxp3
CTLA-4
Animal model
Issue Date: Oct-2009
Publisher: Elsevier Masson SAS
Journal Title: Microbes and Infection
Volume: 11
Issue: 12
Start Page: 964
End Page: 972
Publisher DOI: 10.1016/j.micinf.2009.06.007
PMID: 19596078
Abstract: Human T-cell leukemia virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia (ATL). Some ATL cells express Foxp3, which is known as regulatory T cell (Treg cell) specific transcription factor. It is suggested that Treg cell like suppressive activity of Foxp3 expressing ATL cells is associated to ATL development and related immunodeficiency. To develop an HTLV-I model system that enables to investigate the association of Treg function in ATL progression, we examined the expression of Foxp3 and CTLA-4, Treg cell-associated factor, in established HTLV-1-infected rat cell lines and their regulatory function. We found the expression of Foxp3 in 10 of 22 and CTLA-4 in 10 of 19 HTLV-1-infected rat cell lines. Moreover, some of the Foxp3 and/or CTLA-4 expressing cell lines suppressed proliferation of naïve T cells that were stimulated with anti-CD3 antibody. Particularly all Foxp3+ CTLA-4+ cells showed the suppressive activity. Our data suggest the usefulness of our rat model systems for further analysis of the role of Treg cell-associated factors on the development of ATL and related immunodeficiency in vivo.
Type: article (author version)
URI: http://hdl.handle.net/2115/39626
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 志田 壽利

Export metadata:

OAI-PMH ( junii2 , jpcoar_1.0 )

MathJax is now OFF:


 

 - Hokkaido University