Matsuoka, Masao

Ohshima, Koichi

Satou, Yorifumi

Taguchi, Nanae

Retrovirology

English

PubMed

Nanae Taguchi

Yorifumi Satou

Koichi Ohshima

Masao Matsuoka

Springer - Publisher Connector

HTLV-1 bZIP factor induces systemic inflammations in vivo

MEETING ABSTRACT Open Access
HTLV-1 bZIP factor induces systemic
inflammations in vivo
Nanae Taguchi1*, Yorifumi Satou1, Koichi Ohshima2, Masao Matsuoka1
From 15th International Conference on Human Retroviruses: HTLV and Related Viruses
Leuven and Gembloux, Belgium. 5-8 June 2011
Human T-cell leukemia virus type 1 (HTLV-1) causes
both neoplastic and inflammatory diseases, which
include HTLV-1 associated myelopathy/tropic spastic
paraparesis and uveitis. Recently, we have reported that
transgenic expression of HTLV-1 bZIP factor (HBZ) in
CD4+ T cells caused dermatitis and alveolitis in mice.
In this study, we investigated the production of cyto-
kines in HBZ transgenic (HBZ-Tg) mice to elucidate the
mechanism of its pro-inflammatory phenotype. IFN-g
production in CD4+ T cells was remarkably increased in
splenocytes, lungs and PBMCs from HBZ-Tg compared
with non-transgenic littermates, whereas there was no
difference in levels of IL-4 and IL-17. We also found
that production of IFN-g was remarkably enhanced in
CD4+Foxp3- fraction.
Recent studies have reported that CD4+Foxp3+ T
cells are not terminally differentiated but have a plasti-
city to convert to other T cell subsets. Induced regula-
tory T cells (iTreg) tend to lose Foxp3 expression, and
may acquire an effector phenotype accompanied by the
production of inflammatory cytokines, such as IFN-g.
We observed that the percentage of naturally occurring
Treg cells was lower in HBZ-Tg mice than non-Tg
mice, although total number of Treg was increased in
HBZ-Tg mice. It is suggested that the enhanced genera-
tion of iTreg cells and instability of Foxp3 expression in
HBZ-induced iTreg is a possible mechanism for
increased number IFN-g producing cells in HBZ-Tg
mice, leading to systemic inflammation.
Author details
1Institute for Virus Research, Kyoto University, Kyoto, 606-8507, Japan.
2Department of Pathology, Kurume University School of Medicine, Kurume,
830-0011, Japan.
Published: 6 June 2011
doi:10.1186/1742-4690-8-S1-A8
Cite this article as: Taguchi et al.: HTLV-1 bZIP factor induces systemic
inflammations in vivo. Retrovirology 2011 8(Suppl 1):A8.
Submit your next manuscript to BioMed Central
and take full advantage of: 
• Convenient online submission
• Thorough peer review
• No space constraints or color figure charges
• Immediate publication on acceptance
• Inclusion in PubMed, CAS, Scopus and Google Scholar
• Research which is freely available for redistribution
Submit your manuscript at 
www.biomedcentral.com/submit
* Correspondence: ntaguchi@virus.kyoto-u.ac.jp
1Institute for Virus Research, Kyoto University, Kyoto, 606-8507, Japan
Full list of author information is available at the end of the article
Taguchi et al. Retrovirology 2011, 8(Suppl 1):A8
http://www.retrovirology.com/content/8/S1/A8
© 2011 Taguchi et al; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited.


Crossref

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3112796

HTLV-1 bZIP factor induces systemic inflammations in vivo

Abstract

Similar works

Full text

Available Versions

Springer - Publisher Connector

Springer - Publisher Connector

Crossref