New mechanisms by which complementýregulates the pathogenesis of experimental autoimmune uveitis

补体调节实验性自身免疫性葡萄膜炎发病机制的新机制

基本信息

  • 批准号:
    10397686
  • 负责人:
  • 金额:
    $ 39.04万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2021
  • 资助国家:
    美国
  • 起止时间:
    2021-05-01 至 2025-04-30
  • 项目状态:
    未结题

项目摘要

Abstract Autoimmune uveitis, a common cause of blindness, has an unknown etiology and no known cure. We have been studying experimental autoimmune uveitis (EAU) induced in mice deficient in various complement components, inhibitors, or receptors following active immunization with a retinal antigen and the adoptive transfer of already primed retinal antigen-specific T cells. Our findings strongly suggest that complement, particularly the complement receptors C3aR and C5aR, are required for not only the priming of autoreactive T cells in the periphery, but also the migration and/or re-stimulation of already activated pathogenic T cells in the retina. These findings suggest that these complement receptors could be new therapeutic targets for treating EAU and, eventually, autoimmune uveitis. In this proposed work, we will focus on the previously unknown role of complement in regulating the migration and/or re-stimulation of already primed autoreactive T cells in a target tissue, using EAU as a model. We will also elucidate the underlying mechanisms using various systemic and cell-specific complement-related gene knockout mice and other novel reagents. In addition, we will examine the efficacies and investigate the underlying mechanisms of our novel complement-targeted reagents for suppressing the migration and re- stimulation of previously activated uveitogenic T cells in the retina for the treatment of EAU both in mice and in rats. These studies will significantly improve our understanding of the pathogenesis of autoimmune uveitis and facilitate the development of novel complement-targeted therapeutics for the treatment of this blinding disease.
摘要

项目成果

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FENG C LIN其他文献

FENG C LIN的其他文献

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{{ truncateString('FENG C LIN', 18)}}的其他基金

Role of CDCP1 in the pathogenesis of autoimmune uveitis
CDCP1在自身免疫性葡萄膜炎发病机制中的作用
  • 批准号:
    10655755
  • 财政年份:
    2023
  • 资助金额:
    $ 39.04万
  • 项目类别:
Development of a novel antibody-drug conjugate for treating T-cell lymphoma.
开发用于治疗 T 细胞淋巴瘤的新型抗体-药物缀合物。
  • 批准号:
    10545523
  • 财政年份:
    2022
  • 资助金额:
    $ 39.04万
  • 项目类别:
Development of a new drug for treating autoimmune uveitis
治疗自身免疫性葡萄膜炎新药的研制
  • 批准号:
    10321980
  • 财政年份:
    2021
  • 资助金额:
    $ 39.04万
  • 项目类别:
New mechanisms by which complementýregulates the pathogenesis of experimental autoimmune uveitis
补体调节实验性自身免疫性葡萄膜炎发病机制的新机制
  • 批准号:
    10175270
  • 财政年份:
    2021
  • 资助金额:
    $ 39.04万
  • 项目类别:
New mechanisms by which complementýregulates the pathogenesis of experimental autoimmune uveitis
补体调节实验性自身免疫性葡萄膜炎发病机制的新机制
  • 批准号:
    10619536
  • 财政年份:
    2021
  • 资助金额:
    $ 39.04万
  • 项目类别:
A novel regulator of Pseudomonas aeruginosa keratitis
铜绿假单胞菌角膜炎的新型调节剂
  • 批准号:
    10618396
  • 财政年份:
    2020
  • 资助金额:
    $ 39.04万
  • 项目类别:
A novel regulator of Pseudomonas aeruginosa keratitis
铜绿假单胞菌角膜炎的新型调节剂
  • 批准号:
    10401830
  • 财政年份:
    2020
  • 资助金额:
    $ 39.04万
  • 项目类别:
A novel regulator of corneal wound healing and Pseudomonas aeruginosa keratitis
角膜伤口愈合和铜绿假单胞菌角膜炎的新型调节剂
  • 批准号:
    9898378
  • 财政年份:
    2019
  • 资助金额:
    $ 39.04万
  • 项目类别:
A novel regulator of corneal wound healing and Pseudomonas aeruginosa keratitis
角膜伤口愈合和铜绿假单胞菌角膜炎的新型调节剂
  • 批准号:
    10391450
  • 财政年份:
    2019
  • 资助金额:
    $ 39.04万
  • 项目类别:
A novel regulator of corneal wound healing and Pseudomonas aeruginosa keratitis
角膜伤口愈合和铜绿假单胞菌角膜炎的新型调节剂
  • 批准号:
    10133084
  • 财政年份:
    2019
  • 资助金额:
    $ 39.04万
  • 项目类别:

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ATTAC 时间:针对 gp100 细胞的 T 细胞过继转移来治疗 LAM
  • 批准号:
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  • 批准号:
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Phase I clinical trial of adoptive transfer of autologous folate receptor-alpha redirected CAR T cells for ovarian cancer
自体叶酸受体-α重定向CAR T细胞过继转移治疗卵巢癌的I期临床试验
  • 批准号:
    10387023
  • 财政年份:
    2022
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Determining mechanisms of enhanced antitumor efficacy of four-day expanded Th17 cells for adoptive transfer
确定用于过继转移的四天扩增 Th17 细胞增强抗肿瘤功效的机制
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A phase I clinical study of adoptive transfer of regulatory T cells (Tregs) and low-dose interleukin-2 (IL-2) for the treatment of chronic graft-versus-host disease (GVHD): gene-marking to inform rational combination therapy
调节性 T 细胞 (Treg) 和低剂量白细胞介素 2 (IL-2) 过继转移治疗慢性移植物抗宿主病 (GVHD) 的 I 期临床研究:基因标记为合理的联合治疗提供信息
  • 批准号:
    nhmrc : GNT1163111
  • 财政年份:
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  • 项目类别:
    Project Grants
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确定用于过继转移的四天扩增 Th17 细胞增强抗肿瘤功效的机制
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基因编辑的淋巴祖细胞用于过继转移作为原发性免疫缺陷的治疗
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