Exacerbation of autoimmune arthritis by copolymer-I through promoting type 1 immune response and autoantibody production.

Abstract

Copolymer-I (COP-I) is an unique immune regulatory polymer that has been shown to suppress experimental autoimmune encephalomyelitis (EAE) and is a treatment option for multiple sclerosis (MS). To investigate whether its immune suppressive effects can be extended to other autoimmune diseases, we treated mice with COP-I during the induction of collagen-induced arthritis (CIA). Our results show that COP-I treatment exacerbated CIA, leading to faster onset, more severe and longer-lasting disease. The mechanisms underlying the exacerbation of CIA by COP-I treatment include enhanced activation and inflammatory cytokine production by autoreactive T cells and elevated production of autoreactive antibodies. In addition, germinal center response was significantly enhanced by COP-I treatment. Thus, great caution should be taken when COP-I is to be used in MS patients with other autoimmune complications or its potential therapeutic effects are to be extended beyond autoimmune demyelinating diseases.

• Authors: Biao Zheng, Kirsten Switzer, Ekaterina Marinova, Jinwu Zhang, Shuhua Han
• Journal: Autoimmunity (Autoimmunity) Vol. 41 Issue 5 Pg. 363-71 (Aug 2008) ISSN: 1607-842X [Electronic] England
• PMID: 18568641 (Publication Type: Journal Article)

Chemical References

• Autoantibodies
• Immunosuppressive Agents
• Peptides
• Interleukin-10
• Interleukin-4
• Glatiramer Acetate
• Interferon-gamma
• Collagen

Topics

• Animals
• Arthritis, Experimental (chemically induced, immunology, pathology)
• Autoantibodies (biosynthesis)
• Autoimmune Diseases (drug therapy, immunology, pathology)
• Collagen (immunology)
• Germinal Center (drug effects)
• Glatiramer Acetate
• Immunity, Cellular
• Immunosuppressive Agents (adverse effects)
• Interferon-gamma (biosynthesis)
• Interleukin-10 (biosynthesis)
• Interleukin-4 (biosynthesis)
• Male
• Mice
• Mice, Inbred DBA
• Peptides (adverse effects)
• T-Lymphocytes, Regulatory (drug effects)
• Th1 Cells (drug effects)