Studies of the metabolic regulation of the MICA, a ligand for the innate immune receptor NKG2D

MICA（先天免疫受体 NKG2D 的配体）的代谢调节研究

• 批准号: G0901998/1
• 负责人: Michael McCarthy
• 金额: $ 24.91万
• 依托单位: University of Oxford
• 依托单位国家: 英国
• 项目类别: Fellowship
• 财政年份: 2010
• 资助国家: 英国
• 起止时间: 2010 至 无数据
• 项目状态: 已结题
• 来源: https://gtr.ukri.org/projects?ref=G0901998%2F1
• 关键词: Studies; metabolic; regulation; MICA; ligand

How the immune system recognizes diseased cells is not fully understood. In particular, we do not completely understand how the immune system identifies diseased cells, such as tumour or virus-infected cells, when it has not previously met this particular disease. We are born with this immunity, which is termed innate immunity and does not require previous exposure to the disease. Cancer cells and virus-infected cells display danger makers on their surfaces which flag them as diseased. The immune system can then recognize them and destroy them. We are studying these molecular flags that diseased cells display on their surfaces to identify themselves as diseased and in need of destruction. We have evidence that changes in the metabolism of a diseased cell can be sensed by the cell and cause the cell to put danger markers on its surface. We aim to understand this process in more detail and to identify the different molecules involved. The molecules involved may be useful targets for drugs. In particular, enhancing this immunity could promote the body‘s defence against cancers or infections or help to promote better responses to vaccines. Conversely, inhibiting this immunity could be helpful in autoimmune diseases or transplant rejection.

免疫系统如何识别患病细胞尚未完全了解。特别是，当以前没有遇到这种特定疾病时，我们并不完全了解免疫系统如何鉴定患病细胞，例如肿瘤或病毒感染的细胞。我们天生具有这种免疫学，该免疫学称为先天免疫学，不需要以前接触该疾病。癌细胞和病毒感染的细胞在其表面上显示危险制造者，这些危险将其标记为识别。然后，免疫系统可以识别它们并摧毁它们。我们正在研究这些分子标志，这些标志在其表面上显示出的分子标志，以将自己识别为辨别并需要破坏。我们有证据表明，细胞可以感觉到解剖细胞的代谢的变化，并导致细胞在其表面施加危险标记。我们的目标是更详细地了解这一过程，并确定所涉及的不同分子。涉及的分子可能是药物的有用靶标。特别是，增强这种免疫峰可以促进人体对癌症或感染的防御，或帮助促进对疫苗的更好反应。相反，抑制这种免疫接触可能有助于自身免疫性疾病或移植排斥。