ROLE OF CYTOKINES IN THE DEVELOPMENT OF MAIDS

细胞因子在 MAID 发育中的作用

• 批准号: 2460157
• 负责人: OSAMI KANAGAWA
• 金额: $ 31.53万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1995
• 资助国家: 美国
• 起止时间: 1995-08-04 至 1999-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2460157
• 关键词: AIDS; cytokine; disease /disorder model; gene targeting; genetically modified animals; helper T lymphocyte; immune system; interleukin 4; laboratory mouse; murine AIDSs; murine leukemia virus; pathologic process; virus infection mechanism

DESCRIPTION (Adapted from the applicant's abstract) Murine acquired immunodeficiency syndrome (MAIDS) is caused by a defective murine leukemia virus. The development of the MAIDS requires the presence of CD4 positive T cells and mature B cells. A helper free MAIDs virus which lacks the capacity to produce infectious virus in vivo was shown to be pathogenic. Furthermore, virus infected B cells stimulated syngeneic T cells in vitro. These results strongly suggest that the virus immune system interaction rather than the direct effect of virus infection play a key role in MAIDS. MAIDS is characterized by a development of lymphoadenopathy, polyclonal B cell activation, hypergammaglobulinemia and profound immunodeficiency in both T and B cells. Some of these symptoms are similar to those found in human Aids. Recent analysis demonstrated additional features shared by MAIDs and HIV infection which include involvement of superantigen, the cytokines produced by T cells and programmed lymphocytes death. These findings indicate that, despite the fundamental difference between two viruses, the mechanisms by which virus induces a variety of symptoms, especially immunodeficiency in T cells, may be shared. The long term goal of the study is to understand the MAIDS virus - immune system interaction in the development of the imunodeficiency. Understanding of the pathogenicity of the MAIDs virus will contribute to the understanding of general retrovirus induced diseases, including HIV infection in man.

描述（改编自申请人摘要） 免疫缺陷综合征（MAIDS）是由一种有缺陷的鼠 白血病病毒 MAIDS的发展需要以下方面的存在： CD 4阳性T细胞和成熟B细胞。 一个助手免费MAIDS病毒， 缺乏在体内产生感染性病毒的能力， 致病的 此外，病毒感染的B细胞刺激同系T细胞 体外细胞 这些结果有力地表明， 系统交互作用而不是病毒感染的直接作用 在女仆中扮演重要角色。 MAIDS的特点是发展 淋巴结病，多克隆B细胞活化，高丙种球蛋白血症 以及T和B细胞的严重免疫缺陷。 其中一些 症状与人类艾滋病相似。 最近的分析 证明了MAIDS和HIV感染所共有的其他特征， 包括超抗原的参与，T细胞产生的细胞因子 和程序性淋巴细胞死亡。 这些发现表明， 尽管两种病毒之间存在根本差异，但其机制 病毒通过该途径引起多种症状，尤其是免疫缺陷 在T细胞中，可以共享。 这项研究的长期目标是 了解MAIDS病毒-免疫系统相互作用 免疫缺陷的发展。 对致病性的认识 MAIDS病毒的研究将有助于了解一般的 逆转录病毒引起的疾病，包括人类艾滋病毒感染。