Abstract | OBJECTIVE: METHODS:
Experimental autoimmune myositis was induced in SJL/J mice by immunization with rabbit myosin. Am80 was administered orally once daily. Its effects were evaluated by measurement of the numbers of infiltrating inflammatory cells, production of inflammatory cytokines in muscle, production of Th-specific cytokines by myosin-stimulated splenic T cells, and production of antimyosin antibodies in serum. RESULTS: In mice with experimental autoimmune myositis, orally administered Am80 significantly reduced the number of infiltrating inflammatory cells and the expression of tumor necrosis factor alpha and interleukin-1beta (IL-1beta) in muscle. Moreover, Am80 increased production of interferon-gamma, IL-4, and IL-10, but not IL-17, by myosin-stimulated splenic T cells of mice with experimental autoimmune myositis, suggesting that it could enhance differentiation into Th1 and Th2, but not Th17, in vivo. Am80 also decreased serum levels of IgG2a and IgG2b antimyosin antibodies, but did not affect levels of IgG1 antimyosin antibodies. In addition, it suppressed chemokine expression and activator protein 1 activity in myoblasts in vitro. CONCLUSION:
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Authors | Naho Ohyanagi, Miwako Ishido, Fumihito Suzuki, Kayoko Kaneko, Tetsuo Kubota, Nobuyuki Miyasaka, Toshihiro Nanki |
Journal | Arthritis and rheumatism
(Arthritis Rheum)
Vol. 60
Issue 10
Pg. 3118-27
(Oct 2009)
ISSN: 0004-3591 [Print] United States |
PMID | 19790078
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antibodies
- Benzoates
- Immunoglobulin G
- Interleukin-1beta
- Retinoids
- Tetrahydronaphthalenes
- Transcription Factor AP-1
- Tumor Necrosis Factor-alpha
- tamibarotene
- Myosins
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Topics |
- Animals
- Antibodies
(metabolism)
- Benzoates
(pharmacology)
- Cell Differentiation
(drug effects)
- Disease Models, Animal
- Immunoglobulin G
(metabolism)
- Interleukin-1beta
(metabolism)
- Male
- Mice
- Mice, Mutant Strains
- Myosins
(immunology)
- Nervous System Autoimmune Disease, Experimental
(drug therapy, immunology, prevention & control)
- Retinoids
(pharmacology, therapeutic use)
- T-Lymphocytes, Helper-Inducer
(drug effects, metabolism, pathology)
- Tetrahydronaphthalenes
(pharmacology)
- Th1 Cells
(drug effects, metabolism, pathology)
- Th2 Cells
(drug effects, metabolism, pathology)
- Transcription Factor AP-1
(metabolism)
- Tumor Necrosis Factor-alpha
(metabolism)
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