Therapeutic effects of antibodies to tumor necrosis factor-α, interleukin-6 and cytotoxic T-lymphocyte antigen 4 immunoglobulin in mice with glucose-6-phosphate isomerase induced arthritis 英文参考文献.docVIP
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Therapeutic effects of antibodies to tumor necrosis factor-α, interleukin-6 and cytotoxic T-lymphocyte antigen 4 immunoglobulin in mice with glucose-6-phosphate isomerase induced arthritis 英文参考文献
Available online /content/10/3/R66
Research article
Open Access
Vol 10 No 3
Therapeutic effects of antibodies to tumor necrosis factor-α,
interleukin-6 and cytotoxic T-lymphocyte antigen 4
immunoglobulin in mice with glucose-6-phosphate isomerase
induced arthritis
Isao Matsumoto1,2, Hua Zhang1,2, Takanori Yasukochi1,2, Keiichi Iwanami1, Yoko Tanaka1,
Asuka Inoue1, Daisuke Goto1, Satoshi Ito1, Akito Tsutsumi1 and Takayuki Sumida1
1Division of Clinical Immunology, Major of Advanced Biomedical Applications, Graduate School of Comprehensive Human Sciences, University of
Tsukuba, Tennodai, Tsukuba 305-8575, Japan
2PRESTO, Japan Science and Technology Agency, 4-1-8 Honcho Kawaguchi, Saitama 332-0012, Japan
Corresponding author: Isao Matsumoto, ismatsu@md.tsukuba.ac.jp
Received: 16 Jan 2008 Revisions requested: 13 Feb 2008 Revisions received: 2 May 2008 Accepted: 5 Jun 2008 Published: 5 Jun 2008
Arthritis Research Therapy 2008, 10:R66 (doi:10.1186/ar2437)
This article is online at: /content/10/3/R66
? 2008 Matsumoto et al.; licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
Abstract
Introduction
Immunization
with
glucose-6-phosphate
Results Large amounts of TNF-α and IFN-γ and small amounts
isomerase (GPI) induces severe arthritis in DBA/1 mice. The
present study was designed to identify the cytokines and co-
stimulatory molecules involved in the development of GPI-
induced arthritis.
of IL-2 and IL-6 were produced by splenocytes from mice with
GPI-induced
arthritis.
Anti-TNF-α
mAbs
and
CTLA-4Ig
suppressed TNF-α production, whereas anti-IFN-γ mAbs, anti-
IL-12 mAbs, and CTLA-4 Ig inhibited IFN-γ production. A single
injection of anti-TNF-α and anti-IL-6 mAbs and two injections of
CTLA-4Ig reduced the severity of ar
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