ACR Meeting Abstracts

ACR Meeting Abstracts

Abstract Number: 1952

The Effect of CXCL10 Blockade in C Protein-Induced Myositis

Jinhyun Kim1, Jiyong Choi2, Sung Hae Chang3, Ki Chul Shin4, Sung-Hye Park5, Hye Won Kim6, Hye Jin Oh4, Myeong Jae Yoon7, Bong Seung Ku8, Eun Young Lee6, Eun Bong Lee3, Hiroshi Kawachi9, Hitoshi Kohsaka10 and Yeong Wook Song11, 1Department of Internal medicine, Chungnam National University School of Medicine, Daejeon, South Korea, 2Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea, 3Division of Rheumatology, Department of Internal Medicine, Seoul National University Hospital, Seoul, South Korea, 4Rheumatology, Seoul National University College of Medicine, Seoul, South Korea, 5Department of Pathology, Seoul National University College of Medicine, Seoul, South Korea, 6Division of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea, 7Department of Internal Medicine, School of Medicine, Seoul National University, Seoul, South Korea, 8Rheumatology, Department of Internal Medicine, School of Medicine, Seoul National University Hospital, Seoul, Korea, Seoul, South Korea, 9Department of Cell Biology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan, 10Department of Medicine and Rheumatology, Tokyo Medical and Dental University, Tokyo, Japan, 11Division of Rheumatology, Department of Internal Medicine, Seoul National University, Seoul, South Korea

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords:

Session Information

Title: Muscle Biology, Myositis and Myopathies: Genetics, Autoantibodies and other Molecular Aspects of Idiopathic Inflammatory Myopathies and Models

Session Type: Abstract Submissions (ACR)

Background/Purpose: 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 disease such as RA and SLE. 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 in muscle tissue. 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 inflammation in muscle tissue 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 increased CXCR3+CD4+ T cells (normal mice, 14.14%±1.09% vs. C protein-induced myositis, 37.50%±5.63%) and CXCR3+CD8+ T cells (normal mice, 35.55±2.41% vs. C protein-induced myositis, 79.00%±0.89%) in C protein-induced myositis. 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.

Disclosure:

J. Kim,
None;

J. Choi,
None;

S. H. Chang,
None;

K. C. Shin,
None;

S. H. Park,
None;

H. W. Kim,
None;

H. J. Oh,
None;

M. J. Yoon,
None;

B. S. Ku,
None;

E. Y. Lee,
None;

E. B. Lee,
None;

H. Kawachi,
None;

H. Kohsaka,

Chugai Pharma, Ajinomoto Pharma & Teijin Parma,

5;

Y. W. Song,
None.

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