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IgA mediated Activation of FcalphaRI, an Fc receptor and a Leukocyte Ig-like Receptor.

IgA mediated Activation of FcalphaRI, an Fc receptor and a Leukocyte Ig-like Receptor.
IgA 介导 FcalphaRI、Fc 受体和白细胞 Ig 样受体的激活。
批准号:
nhmrc : 315525
负责人:
A/Pr Mark Wright
金额:
$35.71万
依托单位国家:
澳大利亚
项目类别:
NHMRC Project Grants
财政年份:
2005
资助国家:
澳大利亚
项目状态:
已结题
起止时间:
2005-01-01 至 2007-12-31

项目摘要

项目成果

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中文摘要
翻译
我们的免疫系统的存在是为了寻找和摧毁由细菌和病毒(病原体)引起的感染,这些感染将在我们体内生长。免疫系统中的B细胞制造抗体标签,这些抗体标签附着在病原体上,标记它们以消除它们。一种特殊类型的抗体是IgA。免疫球蛋白有两种形式,第一种是在粘膜部位,这些是体内的膜性通道,如肺、肠道和生殖道。它们与外界沟通,是病原体进入体内的主要途径。在这里,IgA形成了一种相当被动的、但病原体特有的粘性屏障,以防止微生物病原体附着在这些大表面上。在日常的类比中,这种IgA的行为有点像飞纸。这种低调的反应是恰当的,因为我们经常接触生活在我们肠道或呼吸到我们肺部的微生物,如果它侵袭我们无害的微生物邻居,我们的免疫系统会让我们生病。第二种类型的IgA是在血液中发现的,它附着在突破身体屏障的病原体上。这些IgA标签是白细胞积极寻找的,其功能是通过识别和吞噬标记的病原体并用包括漂白剂在内的杀手分子摧毁它们来保护身体免受感染。IgA-Fc受体是白细胞表面的传感器,当它们附着在病原体上时,它会寻找IgA标签。为了在这种恶劣的环境中生存,我们的一些病原体,如葡萄球菌,有自己的策略,使自己对免疫系统不可见。这些策略包括切断IgA标签或阻断IgA的传感器。在这个项目中,我们将研究IgA标签如何打开白细胞来消灭病原体。我们还将研究两种金黄色葡萄球菌蛋白,它们阻断了IgA标签的传感器。最后,我们正在努力了解为什么粘膜型IgA不会像血液中的IgA那样激活白细胞。
英文摘要
Our immune system exists to seek and destroy infections caused by bacteria and viruses (pathogens) that would grow in us. B cells in the immune system make antibody tags which attach to pathogens marking them for elimination. A special type of antibody is IgA. IgA occurs in two forms, the first is found at mucosal sites, these are membranous passages in the body, such as the lung, the gut and the genital tract. These communicate with the outside and are the major route of pathogen entry into the body. Here IgA forms a rather passive, but pathogen specific, sticky barrier to prevent microbial pathogens attaching to these large surfaces. In an everyday analogy this IgA behaves somewhat like fly-paper. This subdued response is appropriate as we are constantly exposed to micro-organisms living in our gut, or breathed into our lungs, and our immune system would make us ill if it aggressively attacked our innocuous microbial neighbours. The second type of IgA is found in the blood where it attaches to pathogens that have breached the body's barriers. These IgA tags are actively sought by white blood cells whose function is to protect the body from infection by recognising and engulfing the tagged pathogens and destroying them with killer molecules, including bleach. The IgA-Fc receptor is the sensor on the surface of white blood cells which seeks the IgA tags as they attach to pathogens. In order to survive in this hostile environment some of our pathogens, such as Staphylococcus, have their own strategies to make themselves invisible to the immune system. These strategies include cutting up the IgA tags or blocking the sensors for IgA. In this project we will study how IgA tags turn on white blood cells to destroy pathogens. We will also be looking at two Staphylococcal proteins which block up the sensor for IgA tags. Finally we are endeavouring to understand how it is the mucosal type IgA does not activate the white cells nearly as much as the IgA from the blood.
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THE ROLE OF THE TETRASPANINS CD37 AND CD82 IN LEUKOCYTE MIGRATION
  • 批准号:
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  • 资助金额:
    $24.73万
  • 财政年份:
    2012
  • 负责人:
    A/Pr Mark Wright
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  • 项目类别:
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  • 资助金额:
    $27.95万
  • 财政年份:
    2009
  • 负责人:
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  • 依托单位:
Molecular interactions of the tetraspanins CD37, TSSC6 and CD151 in T cells
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    nhmrc : 315405
  • 项目类别:
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    $37.78万
  • 财政年份:
    2005
  • 负责人:
    A/Pr Mark Wright
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