2003 Fiscal Year Final Research Report Summary
Evidence against epitope spreading of T cells in autoimmune diseases.
| Project/Area Number |
14370161
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
内科学一般
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| Research Institution | The University of Tokyo |
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Principal Investigator |
YAMAMOTO Kazuhiko The University of Tokyo, Faculty of Medicine, Professor, 医学部附属病院, 教授 (80191394)
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| Co-Investigator(Kenkyū-buntansha) |
KOMAGATA Yoshinori The University of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (60281995)
MISAKI Yoshiikata The University of Tokyo, Faculty of Medicine, Lecturer, 医学部附属病院, 講師 (60219615)
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| Project Period (FY) |
2002 – 2003
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| Keywords | autommune disease / epitope / T cells / T cell receptor / pathogenic T cell |
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| Research Abstract |
Epitope spreading is a well known phenomenon of autoimrnune process especially in the induction phase of the diseases. We examine whether this phenomenon is also working in the stage of advanced phase of autoimmune disorders. We have examined accumulated T cells clones in the several organs of spontaneous models of autoimmune disorders by RT PCR/SSCP analysis of T cell receptor. We found that there are extensive accumulations of T cells in the lesions of late phase animals and the same clones exist in the different pathological lesions of kidney, lung and central nervous system of such animals. We then constructed cDNA library from a single cell isolated from the lesions and obtained fill length cDNAs encoding alpha and beta chains of T cell receptor. After identification of the in vivo accumulated clones to the cloned T cell receptors, cytokine messages were examined using the cDNA library. Some clones were found to express interferon gamma message, suggesting that such clones were pathogenic T cells. We are now trying to reconstitute T cell receptor function by retroviral gene transfer in order to know the pathogenic properties of such clones.
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[Publications] Tokuhin o S, Yamada R, Chang X, Suzuki A, Koch Y, Sawada T, Suzuki M, Nagasaki M, Ohtsuki M, Olio M, Furukawa H, Nagashima M, Yoshino S, Mabuchi A, Sekine A, Saito S, Takahashi A, Tunoda T, Nakamura Y, Yamamoto K.: "An intronic SNP in a RUNXI binding site of SLC22A4, encoding an organic cation transporter, is associated with rheumatoid arthritis"Nature Gene. 35. 341-348 (2003)
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「研究成果報告書概要(欧文)」より
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[Publications] Suzuki A, Yamada R, Chang X, Tokuhiro S, Sawada T, Suzuki M, Nagasaki M, Nakayama-Hamada M, Kawaida R, Ono M, Ohtsuki M, Furukawa H, Yoshino S, Yukioka M, Tohma S, Matsubara T, Wakitani S, Teshima R, Nishioka Y, Sekine A, Iida A, Takahashi A, Thunoda T, Nakamura Y, Yamamoto K: "Functional haplotypes of PAD14, encoding citnullinating enzyme peptidylarginine deiminase 4, are associated with rheumatoid arthritis"Nature Genet. 34. 395-402 (2003)
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「研究成果報告書概要(欧文)」より
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[Publications] Sekiya T, Tsunemi Y, Miyamasu M, Ohta K, Morita A, Saeki H, Matsushima K, Yoshie O, Tuchiya N, Yamaguchi M, Yamamoto K, Tamaki K, Hirai K.: "Variations in the human Th2-specific chemokine TARC gene"Immunogenetics. 54. 742-745 (2003)
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「研究成果報告書概要(欧文)」より
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[Publications] Takanii K, Takuwa N, Okazaki H, Kobayashi M, Ohtoshi T, Kawasaki S, Dohi M, Yamamoto K, Nakamura T, Tanaka M, Nakahara K, Takuwa Y, Takizawa H.: "Interferon-γ inhibits hepatocyte growth factor-simulated cell proliferation of human bronchial epithelial cells upregulation of p27^<kip1> cyclin-dependent kinase inhibitor."Am J Respir Cell Mol Biol. 26. 231-238 (2002)
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