| Project/Area Number |
07557121
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 試験 |
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| Research Field |
病態科学系歯学(含放射線系歯学)
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| Research Institution | The University of Tokushima |
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Principal Investigator |
HAYASHI Yoshio Department of Pathology, School of Dentistry, The University of Tokushima, Professor, 歯学部, 教授 (00127854)
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| Co-Investigator(Kenkyū-buntansha) |
HAMANO Hironori Department of Pathology, School of Dentistry, The University of Tokushima, Resea, 歯学部, 助手 (10238074)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥16,100,000 (Direct Cost: ¥16,100,000)
Fiscal Year 1996: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 1995: ¥12,100,000 (Direct Cost: ¥12,100,000)
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| Keywords | Sjogren's syndrome / Animal model / Cytokine / RT-PCR / Autoantigen / alpha-fodrin / Synthetic peptide / Therapeutic effect / Sjogren′s syndrome / シェ-グレン症候群 / 疾患モデル / 自己抗原ペプチド / 合成ペプチド治療 / T細胞レセプター / サイトカイン / MRL / lprマウス / NFS / sidマウス |
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| Research Abstract |
Primary Sjogren's syndrome in humans is an autoimmune disease of unknown etiology that is characterized by diffuse lymphoid infiltrates in the exocrine organs, such as the salivary and lacrimal glands, but there has not been an appropriate animal model of the human disease. It has been assumed that a combination of immunologic, genetic, and environmental factors may play a key role in development of autoimmune lesions in the salivary and lacrimal glands, but little is known about the disease pathogenesis of primary Sjogren's syndrome. We have established an animal model for primary Sjogren's syndrome in NFS/sld mutant mice bearing an autosomal recessive gene with sublingual differentiation arrest. Severe autoimmune lesions in the salivary and lacrimal glands developed spontaneously in this strain of mice thymectomized 3 day after birth. Such an animal model is essential to study and elucidate the pathogenesis of autoimmune disorders in primary Sjogren's syndrome. More recently, we purified 120KDa organ-specific autoantigen from salivary gland tissues of an NFS/sld animal model. This purified antigen induced proliferative T cell responses, as well as cytokine production including IL-2, and interferon-gamma. Intravenous injection with synthetic peptide prevented the organ-specific autoimmune lesions in mice. We can speculate that the anti-120 KDa immune response play a critical role in the development of primary Sjogren's syndrome.
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