International Immunology Advance Access published online on March 29, 2004
International Immunology, doi:10.1093/intimm/dxh075
© 2004 by The Japanese Society for Immunology
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1 Applied Biological Chemistry, University of Tokyo, Bunkyo, Tokyo 113-8650, Japan; Applied Chemistry, Keio University, Yokohama, Kanagawa 223-8582, Japan; Japan Science and Technology Agency, CREST, Kawaguchi, Saitama 332-0012, Japan; Immune Regulation, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA
* To whom correspondence should be addressed. E-mail: aki{at}educ.cc.keio.ac.jp.
T cell responses directed toward TCR-derived peptides have been shown to be an important regulatory mechanism of protection against autoimmunity. Here, we show that a naturally induced TCR-directed immune response can delay the onset of collagen-induced arthritis (CIA), an animal model of autoimmune rheumatoid arthritis in humans. DBA/1 mice were pretreated with an immunodominant peptide, p245-270, from bovine type II collagen (bCII) and were subsequently immunized with whole bCII for the induction of arthritis. The results showed that preactivation of p245-270-reactive cells delayed the onset and reduced the severity of CIA, compared with animals in the control group. Interestingly, the serum antibody response to bCII and the bCII-specific cytokine were not affected under these conditions. This result indicates that the observed protection was neither directly due to a lower antibody response nor due to the immune deviation of the anti-bCII T cell response. Furthermore, immunization with p245-270, but not bCII, induced a strong response to the B5 peptide, an immunodominant region of the TCR V Keywords:
Keywords: anti-TCR response, collagen-induced arthritis, immune regulation
Accepted February 22, 2004
Article
Vaccination with an immunodominant peptide of bovine type II collagen induces an anti-TCR response, and modulates the onset and severity of collagen-induced arthritis
2 Applied Biological Chemistry, University of Tokyo, Bunkyo, Tokyo 113-8650, Japan; Immune Regulation, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA
3 Applied Biological Chemistry, University of Tokyo, Bunkyo, Tokyo 113-8650, Japan; Research and Development Center, Nippon Meat Packers, Tsukuba, Ibaraki 300-2646, Japan
4 Applied Biological Chemistry, University of Tokyo, Bunkyo, Tokyo 113-8650, Japan
5 Applied Chemistry, Keio University, Yokohama, Kanagawa 223-8582, Japan; Japan Science and Technology Agency, CREST, Kawaguchi, Saitama 332-0012, Japan
6 Immune Regulation, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA
Abstract 
8.2 (amino acids 76-101) that binds very strongly to I-Aq. These data suggest that at a critical phase in the loss of self-tolerance, an effective anti-TCR response, induced naturally, can regulate the pathogenic autoimmune response and thus may provide protection against autoimmunity.
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