Treatment of adjuvant arthritis with granulocyte-colony stimulating factor and peptide derived from heat shock protein 65 |
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Authors: | Brendolan Andrea Higuchi Masanori Sibley Richard Strober Samuel |
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Institution: | Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, CCSR Bldg Rm 2215, CA 94305, USA. |
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Abstract: | Adjuvant arthritis in Lewis rats is induced by the subcutaneous injection of Mycobacterium tuberculosis in mineral oil, and the predominant T cell immune reactivity is against the heat shock protein 65 derived peptide 176-190. We treated Lewis rats with human recombinant G-CSF followed by (i.v) administration of peptide 176-190 after induction of adjuvant arthritis (AA), and observed decreased disease severity, joint destruction, new bone formation and joint ankylosis. Treatment with G-CSF alone was also effective, but to a lesser extent. In addition, we found that splenocytes from rats treated with G-CSF had reduced antigen presenting capacity compared with splenocytes from vehicle treated rats. Primed lymph node cells from G-CSF plus peptide treated rats showed a marked reduction in proliferation and secretion of IFN-gamma after stimulation with the heat shock protein peptide in vitro as compared to controls. |
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Keywords: | Adjuvant arthritis Granulocyte-colony stimulating factor Heat shock protein Immunoregulation |
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