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Cell :白介素-7或可帮助治愈艾滋病
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来自澳大利亚墨尔本大学医学生物学系,霍尔医学研究所,加拿大大学健康网络医院,美国斯坦福大学医学院等处的研究人员利用免疫系统中的一个早已发现的因子:IL-7,来清除小鼠体内的艾滋病病毒,抑制感染,增强小鼠的免疫反应,从而有文章的通讯作者是加拿大大学健康网络医院,多伦多大学生物物理医疗和免疫学系教授Pamela S. Ohashi,Ohashi教授获得过多项免疫学重要研究成果,是免疫学领域的著名科学家。Ohashi教授对于这一最新研究成果信心十足,认为可以在至十五年内找到治愈艾滋病的方法。 白介素-7(IL-7)是一种多效细胞因子,具有广泛的免疫效应,IL-7在T细胞的生长、存活及分化方面有重要作用,同时有潜在趋化性质,介导单核细胞参与炎症反应,近年来IL-7在炎症方面发挥很大的潜在价值,08年的一项研究成果还表明IL-7可以促进癌症免疫反应。 在这篇文章中,研究人员将IL-7注射到小鼠体内,这些感染了人类艾滋病病毒的小鼠,一部分在三个星期内连续注射IL-7,另外一部分则注射其它的激素,结果经过30天后,研究人员惊讶的发现在注射IL-7的小鼠中,T细胞的数量大幅增加,而且60天后,这项小鼠基本上已经清楚了体内病毒。 目前澳大利亚有2万名艾滋病病毒携带病人,已经有超过7000人因感染艾滋病病毒有关的病而死亡,这项病毒与乙肝,丙肝病毒一样,会造成人体免疫系统超负荷,引发慢性感染,这些病患体内的病毒很多,导致免疫系统也放弃了与病毒的对抗,尤其是免疫系统内的T细胞。 研究人员希望在两年后能对艾滋病病患进行实验,也可以采用注射的方向,每三日或每星期为病人注射一次(主要取决于注射的强度),持续约一个月。这样也许就能治愈艾滋病了,这种方法还可能可以用于其它的慢性疾病,比如乙肝和丙肝,以及细菌感染的疾病,比如肺结核等。(Bioon.com) 生物谷推荐原文出处: Cell doi:10.1016/j.cell.2011.01.011 IL-7 Engages Multiple Mechanisms to Overcome Chronic Viral Infection and Limit Organ Pathology Marc Pellegrini, Thomas Calzascia, Jesse G. Toe, Simon P. Preston, Amy E. Lin, Alisha R. Elford, Arda Shahinian, Philipp A. Lang, Karl S. Lang, Michel Morre, Brigitte Assouline, Katharina Lahl, Tim Sparwasser, Thomas F. Tedder, Ji-hye Paik, Ronald A. DePinho, Sameh Basta, Pamela S. Ohashi, Tak W. Mak Highlights Socs3 is upregulated in T cells during chronic active viral infection in mice Deletion of socs3 in T cells prevents immune failure and promotes viral clearance In vivo IL-7 therapy represses Socs3 in T cells and clears chronic infection IL-7 promotes IL-22 production to mitigate immunopathology in chronic infection Summary Understanding the factors that impede immune responses to persistent viruses is essential in designing therapies for HIV infection. Mice infected with LCMV clone-13 have persistent high-level viremia and a dysfunctional immune response. Interleukin-7, a cytokine that is critical for immune development and homeostasis, was used here to promote immunity toward clone-13, enabling elucidation of the inhibitory pathways underlying impaired antiviral immune response. Mechanistically, IL-7 downregulated a critical repressor of cytokine signaling, Socs3, resulting in amplified cytokine production, increased T cell effector function and numbers, and viral clearance. IL-7 enhanced thymic output to expand the naive T cell pool, including T cells that were not LCMV specific. Additionally, IL-7 promoted production of cytoprotective IL-22 that abrogated liver pathology. The IL-7-mediated effects were dependent on endogenous IL-6. These attributes of IL-7 have profound implications for its use as a therapeutic in the treatment of chronic viral diseases.
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