A study of defense mechanism against the infection of intestinal nematode by using knockout mice

利用基因敲除小鼠研究肠道线虫感染的防御机制

• 批准号: 08457081
• 负责人: TADA Isao
• 金额: $ 2.82万
• 依托单位: Kyusyu University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 1996
• 资助国家: 日本
• 起止时间: 1996 至 1997
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08457081/
• 关键词: Strongyloides ratti; Knockout mouse; Mast cell; CD8+T cell; Expulsion; Protective immunity; Testosterone; Macrophage; CD8+T細胞; 防御免疫; 肥満細胞; goblet cell

In the fiscal years 1996 and 1997, aiming at the analysis of the mechanism concerned in the protective immunity against the infection of intestinal nematode, we studied Strongyloides ratti (Sr) infection in the CD45 exon 6-deficient mice (CD45-1-). Following results were obtained :1) In CD45-/-, the protective immunity was markedly reduced and the period of infection lasted remarkably longer than the control.2) Sr infection in CD45-/-inoculated with splenocytes revealed that the marked reduction of protective immunity does not depend only on the T cell dysfunction .3) Induction of mucous mast cells (MMC) by the adiministration of IL-3 did not cause the expulsion in CD45-/- probably bacause of the dysfunction of MMC itself.4) CD8+T cells were considered not essential in the protection against Sr in CD45-/-. The unique character of CD45-/- was shown in this study.5) Influence of testosterone on the macrophage activity in the protection was investigated. The study revealed that testosterone promoted the protection inhibition when the macrophagaes were damaged by carbon.

在1996和1997财政年度，为了分析肠道线虫感染的保护性免疫中有关的机制，我们研究了CD 45外显子6缺陷小鼠（CD 45 -1-）中的棒状圆线虫（Sr）感染。结果表明：（1）CD 45-/-细胞的保护性免疫功能明显降低，感染持续时间明显长于对照组;（2）Sr感染CD 45-/-细胞后，保护性免疫功能的明显降低并不完全依赖于T细胞功能障碍;（3）IL-3诱导的粘液肥大细胞（MMC）并不引起CD 45-/-细胞的排斥，可能是由于MMC自身功能障碍所致;（4）CD 8 +T细胞在CD 45-/-细胞的抗Sr保护中并不起重要作用。本研究显示了CD 45-/-的独特性质。5）研究了睾酮对巨噬细胞活性的影响。研究表明，睾酮促进了碳源对巨噬细胞的保护抑制作用。