The effect of CXCL10 blockade in C protein-induced myositis
Jinhyun
Kim1,
Jiyong
Choi2,
Sunghae
Chang2,
Sung-Hye
Park2,
Kichul
Shin2,
Hye Won
Kim2,
Hyejin
Oh2,
Myeong Jae
Yoon2,
Bon Seung
Ku2,
Eun Young
Lee2,
Eun Bong
Lee2,
Hiroshi
Kawachi3,
Hitoshi
Kohsaka4 and
Yeong-Wook
Song2*
-
1
Chungnam National Univeristy Hospital, Republic of Korea
-
2
Seoul National University College of Medicine, Republic of Korea
-
3
Niigata University Graduate School of Medical and Dental Sciences, Department of Cell Biology, Institute of Nephrology, Japan
-
4
Tokyo Medical and Dental University, Department of Medicine and Rheumatology, Japan
Background: CXCL10 (also called interferon-γ-inducible protein 10 [IP-10]) is a chemokine that plays a critical role in the infiltration of T cell in autoimmune diseases. CXCL10 is reported to be expressed in muscle tissue of polymyositis, thus we investigated the role of CXCL10 and the effect of CXCL10 blockade in C protein-induced myositis, an animal model of polymyositis.
Methods: C protein-induced myositis model was induced with human skeletal C protein fragment in 8-week-old female C57BL/6 mice. Immunohistochemistry was performed to detect CXCL10 and CXCR3, its receptor. CXCR3 in mouse splenocyte was investigated by flow cytometry. Migration assay of mouse splenocyte was performed with 5 μm pore transwell system. Mice with C protein-induced myositis were treated with anti-CXCL10 antibody or control IgG 8 days after the induction of myositis and the muscle inflammation was assessed 3 week after the induction.
Results: Immunohistochemistry showed the expression of CXCL10 and CXCR3 in the muscle of C protein-induced myositis. Flow cytometry demonstrated IFN-γ+ cells were increased among CXCR3+CD8+ T cells compared to CXCR3-CD8+ T cells (CXCR3+CD8+ T cell, 28.0 ± 4.2% vs. CXCR3-CD8+ T cell, 9.5 ± 1.5%, p = 0.016). Migration of splenocyte was increased in response to CXCL10 (chemotactic index=1.91±0.45). Treatment with anti-CXCL10 antibody (n=10) showed less inflammation score in muscles than treatment with control IgG (n=10; median [range], anti IP-10, 0.75 [0.25-2.00] vs. control IgG, 1.43 [1.125-4.25], p=0.045).
Conclusion: CXCL10 was expressed in the inflammation of C protein-induced myositis model and its blockade suppressed inflammation in muscle.
Keywords:
Polymyositis,
CXCL10,
CXCR3,
mouse model,
chemokine
Conference:
15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013.
Presentation Type:
Abstract
Topic:
Immune receptors and signaling
Citation:
Kim
J,
Choi
J,
Chang
S,
Park
S,
Shin
K,
Kim
H,
Oh
H,
Yoon
M,
Ku
B,
Lee
E,
Lee
E,
Kawachi
H,
Kohsaka
H and
Song
Y
(2013). The effect of CXCL10 blockade in C protein-induced myositis.
Front. Immunol.
Conference Abstract:
15th International Congress of Immunology (ICI).
doi: 10.3389/conf.fimmu.2013.02.00747
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Received:
18 Jun 2013;
Published Online:
22 Aug 2013.
*
Correspondence:
Prof. Yeong-Wook Song, Seoul National University College of Medicine, Seoul, Republic of Korea, ysong@snu.ac.kr