| Project/Area Number |
11671819
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Nihon-University |
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Principal Investigator |
KOMTYAMA Kazuo Nihon-University, School of Dentistry, Associate Professor, 歯学部, 助教授 (00120452)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2000: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1999: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | aly / IL-2 / INFγ / RT-PCR / DTH / Th1 / cytokine / oral / IgA欠損 / INF-γ / NK細胞 / SC / NK / cytokine / Th2 |
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| Research Abstract |
The alymphoplasia (aly-/-) mouse has a severe immunodeficiency, because it lacks peripheral lymph nodes as well as immunoglobulin synthesis. In the present study performed histopathological and immunohistological examinations to clarify histological disorders of various immune organs in these mice. T-cells related cytokine mRNA expressions were also examined using RT-PCR Carbon CH40 injections into the tongue confirmed the absence of submandibular lymph nodes. The thymus had a poorly constructed cortex and medulla, and the number of lymphoid follicles was clearly decreased in the spleen. No IgG- or IgA- producing cells were found in any immune organs, including the mucosal immune sites, though a few IgM -producing cells were identified. Other characteristic findings included perivascular lymphocytes accumulation in the salivary glands, lungs, liver and pancreas, which caused tissues damage. The infiltration cells showed CD90+ but CD4- and CD8-. However, CD25 expression was detected after CD3 stimulation. The lymphocyte does not synthesized IL-2 and INFγ mRNA that is one of causes for the various immunodeficiency in aly/aly mouse. The mouse also revealed low levels of the delayed type hypersensitivity. In the elucidation of oral delayed type hypersensitivity on oral buccal mucosa, IL-2 and INFγ from Th1 cells played key molecules for the disease severity. The data confirmed by the deletion of IL-2 and INFγ synthesized cells from C57/BL mice by assialo GM1 treatment experiments. Further study performed to elucidate the organ-specific lymphocyte accumulations in relation to the T-cell functions
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