Fundamental study of T cell related cytokine in alymphoplasia (aly-/-) mouse

发育不全(aly-/-)小鼠T细胞相关细胞因子的基础研究

• 批准号: 11671819
• 负责人: KOMTYAMA Kazuo
• 金额: $ 2.24万
• 依托单位: Nihon-University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671819/
• 关键词: aly; IL-2; INFγ; RT-PCR; DTH; Th1; cytokine; oral; IgA欠損; INF-γ; NK細胞; SC; NK; cytokine; Th2

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

淋巴增生（aly-/-）小鼠具有严重的免疫缺陷，因为它缺乏周围淋巴结以及免疫球蛋白合成。本研究通过组织病理学和免疫组织学检查来阐明这些小鼠各种免疫器官的组织学紊乱。RT-PCR检测了t细胞相关细胞因子mRNA的表达，并将碳CH40注射到舌内，证实了下颌下淋巴结的缺失。胸腺皮质和髓质结构不佳，脾脏淋巴滤泡数量明显减少。在包括粘膜免疫部位在内的任何免疫器官中均未发现产生IgG或IgA的细胞，但发现了少量产生IgM的细胞。其他特征性发现包括唾液腺、肺、肝和胰腺血管周围淋巴细胞积聚，导致组织损伤。浸润细胞显示CD90+，但CD4-和CD8-。然而，CD3刺激后检测到CD25的表达。淋巴细胞不能合成IL-2和INFγ mRNA是导致aly/aly小鼠各种免疫缺陷的原因之一。小鼠也显示出低水平的延迟型超敏反应。在口腔口腔黏膜延迟型超敏反应的研究中，来自Th1细胞的IL-2和INFγ是影响疾病严重程度的关键分子。通过assialo GM1处理C57/BL小鼠的IL-2和INFγ合成细胞的缺失证实了这一数据。进一步的研究阐明了器官特异性淋巴细胞积累与t细胞功能的关系

项目成果

Komiyama K et al: "Histological and immunohistological analysis in IgA deficient a lymphoplasia (aly/aly) mouse"J.Oral Science. 42(掲載予定). (2001)

Komiyama K 等人：“IgA 缺陷型（aly/aly）小鼠的组织学和免疫组织学分析”J. Oral Science 42（即将出版）。

Komiyama, K., Sato, J., Okaue, M., Goto, T., Horimoto, S., Akagi, T., Akima, S., More, I.: "Histological and immunohistological analysis in IgA defecient a lympphoplasia (aly-/-) mouse."J.Oral Science. 42(in press). (2001)

Komiyama, K.、Sato, J.、Okaue, M.、Goto, T.、Horimoto, S.、Akagi, T.、Akima, S.、More, I.：“IgA 缺陷性淋巴组织发育不良的组织学和免疫组织学分析

Komiyama, K., Okaue, M.and Moro, I.: "Cell and cytokine in oral delayed type hepersens-Itivity"Immulogy letters. 69(1). 145 (1999)

Komiyama, K.、Okaue, M. 和 Moro, I.：“口服延迟型 hepersens-Itivity 中的细胞和细胞因子”免疫学信件。

Okae, M.: "Elicitation of delated type hypersensitivity and a kinetic study of infiltrating cells in mouse buccal mucosa"Nihon University Dental Journal. 74(5). 540-549 (2000)

Okae, M.：“迟发型超敏反应的诱发和小鼠颊粘膜浸润细胞的动力学研究”《日本大学牙科杂志》。

岡上真裕: "マウス趙粘膜への遅延型過敏症の誘導および浸潤細胞動態の検討"日大歯学. 74. 540-549 (1999)

Masahiro Okagami：“小鼠粘膜迟发型超敏反应的诱导和浸润细胞动力学的研究”日本大学牙科，74。540-549（1999）