Analysis of T cell function in Agammaglobulinemia-aly/aly mice-

无丙种球蛋白血症-aly/aly小鼠T细胞功能分析-

基本信息

批准号：
09671934
负责人：
KOMIYAMA Kazuo
金额：
$ 2.11万
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：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

项目摘要

Agaminaglobulinemia is serve immunodeficient disease that resulted in a lack of particular immunoglobulins. In current study, we have examined T cell function of aly/aly mice as a model of agammaglobulinemia that the mice revealed a severe combined immunodificiency including a lack of IgA and IgG synthesis. The aly/aly mice are also a lack of Peyer's patches. On the histological examination, the mice revealed unclear margin of medulla and cortex in thymus. The number of follicles in the spleen was reduced in compared with conventional mice. The lymphocytes were isolated from spleen and measured T/B cell ratio by FACS.Aly/aly mice showed normal T/B cell ratios however the total recovered cell numbers were clearly low than conventional mice. In vivo and In vitro antigen stimulation of the aly/aly mice revealed no antibody response. The cytokine profiles of T cells were examined by RT-PCR.We found that IL-2 mRNA synthesis was quite low revels in the aly/aly mice, while other cytokines mRNA syntheses were constantly detected by RT-PCR.The IL-2 receptor expression in T cell was also in low levels. This IL2 deficiency was proved by an anti-CD3 treated cell proliferation assay, ELISA and FACS analysis. The size and number of colony formation after CD3 and PMA stimulation of T cells were decreased. IgM antibody response was recovered after IL2 adding to in vitro antigen stimulation assay. An experiment of mix lymphocyte culture revealed low levels of B cell response. The establishment of T cell clone was not succeeded. The result indicated that agammaglobulinemia of the aly/aly mice may be caused by the deficient of IL2 synthesis in T cells. However, B cell function was also involved in this immunodeficiency. Farther molecular base analysis was required for resolve T cell dysfunction in an agammaglobulinemia.

agaminaglobulinemia是患有免疫缺陷疾病，导致缺乏特定的免疫球蛋白。在当前的研究中，我们研究了ALY/ALY小鼠的T细胞功能，作为AGAMMAGLOBLOBLOBLINEMIA的模型，即小鼠揭示了严重的合并免疫能力，包括缺乏IgA和IgG合成。 Aly/Aly小鼠也缺乏Peyer的补丁。在组织学检查中，小鼠揭示了胸腺中髓质和皮质的不清缘。与常规小鼠相比，脾脏中的卵泡数量减少。从脾脏中分离出淋巴细胞，并通过FACS.ALY/ALY小鼠测量的T/B细胞比率表现出正常的T/B细胞比率，但是总恢复的细胞数量明显低于常规小鼠。 ALY/ALY小鼠的体内和体外抗原刺激显示没有抗体反应。通过RT-PCR检查了T细胞的细胞因子谱。我们发现，在ALY/ALY小鼠中IL-2 mRNA合成的启示非常低，而其他细胞因子MRNA合成则通过RT-PCR经常检测到。T细胞中的IL-2受体表达也很低。抗CD3处理的细胞增殖测定法，ELISA和FACS分析证明了这种IL2缺乏症。 CD3和T细胞PMA刺激后的菌落形成的大小和数量减少。在IL2添加体外抗原刺激测定后，回收IgM抗体反应。混合淋巴细胞培养的实验显示，B细胞反应的水平较低。 T细胞克隆的建立没有成功。结果表明，ALY/ALY小鼠的Agammaglobulinemia可能是由T细胞中IL2合成的缺乏引起的。但是，B细胞功能也参与了这种免疫缺陷。在AGAMMAGLOBLOBLINEMIA中解决T细胞功能障碍需要更远的分子碱基分析。