APOPTOSIS/TOLERANCE/MAINTENANCE OF IMMUNITY

细胞凋亡/耐受/免疫维持

基本信息

  • 批准号:
    2888239
  • 负责人:
  • 金额:
    $ 27.26万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1988
  • 资助国家:
    美国
  • 起止时间:
    1988-04-01 至 2002-03-31
  • 项目状态:
    已结题

项目摘要

DESCRIPTION (Investigator's Abstract): This laboratory has been actively engaged in the study of the eye as an immunologically privileged site using the ACAID model of immunoregulation (ACAID) for Anterior Chamber Associated Immune Deviation). In general, following the introduction of a variety of antigens into the eye, cell mediated responses are actively suppressed, while antibody responses are normal or elevated. It has been shown that this pattern of responses is due to aggressive regulation by various populations of T-cells (10-13) and antigen presenting cells (14). Previous studies from the laboratory have extensively characterized the Ts-cells involved in ACAID, identified a serum borne factor that mediates ACAID, located an antigen presenting cell for TNP-ACAID, identified several cytokines involved in ACAID, and demonstrated that light regulates the suppressed DTH response in ACAID. It is the purpose of these studies to continue this work and further analyze the regulation of the ocular immune response. The investigators will first examine the role of adhesion molecules in the activation of T-cell in the eye. Specifically, T-cell integrins such as VLA-VLA-5, LFA-1, as well as ICAM-1 will be studied by using small synthetic peptides and antibodies that block their function. These types of studies have important implications for drug design. Studies will be done to continue the analysis of the soluble mediators in ACAID. The investigators will also determine the role of T-cell derived cytokine, complement component C5, and soluble T-cell receptor in the ACAID system. In addition, they will look at the regulation of the antibody response following anterior chamber injection of antigen. Understanding the relationship between the immune system and the eye has important implications for the control and treatment of ocular disease.
描述(研究者摘要):本实验室一直处于活跃状态

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)

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Thomas Almon Ferguson其他文献

Thomas Almon Ferguson的其他文献

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{{ truncateString('Thomas Almon Ferguson', 18)}}的其他基金

Modulation of cone photoreceptor function by autophagy
自噬调节视锥光感受器功能
  • 批准号:
    10681018
  • 财政年份:
    2023
  • 资助金额:
    $ 27.26万
  • 项目类别:
Immune Privilege, Müller cells, and Autophagy
免疫特权、Müller 细胞和自噬
  • 批准号:
    10680566
  • 财政年份:
    2022
  • 资助金额:
    $ 27.26万
  • 项目类别:
Immune Privilege, Müller cells, and Autophagy
免疫特权、Müller 细胞和自噬
  • 批准号:
    10501886
  • 财政年份:
    2022
  • 资助金额:
    $ 27.26万
  • 项目类别:
Regulation of Immunity by Dead Cells
死亡细胞对免疫的调节
  • 批准号:
    7060799
  • 财政年份:
    2005
  • 资助金额:
    $ 27.26万
  • 项目类别:
Regulation of Immunity by Dead Cells
死亡细胞对免疫的调节
  • 批准号:
    6878288
  • 财政年份:
    2005
  • 资助金额:
    $ 27.26万
  • 项目类别:
Regulation of Immunity by Dead Cells
死亡细胞对免疫的调节
  • 批准号:
    7409557
  • 财政年份:
    2005
  • 资助金额:
    $ 27.26万
  • 项目类别:
REGULATION OF IMMUNITY BY DEAD CELLS
死亡细胞对免疫的调节
  • 批准号:
    8056821
  • 财政年份:
    2005
  • 资助金额:
    $ 27.26万
  • 项目类别:
Regulation of Immunity by Dead Cells
死亡细胞对免疫的调节
  • 批准号:
    7852063
  • 财政年份:
    2005
  • 资助金额:
    $ 27.26万
  • 项目类别:
Regulation of Immunity by Dead Cells
死亡细胞对免疫的调节
  • 批准号:
    7221200
  • 财政年份:
    2005
  • 资助金额:
    $ 27.26万
  • 项目类别:
CORE-MOLECULAR BIOLOGY
核心分子生物学
  • 批准号:
    6949368
  • 财政年份:
    2005
  • 资助金额:
    $ 27.26万
  • 项目类别:

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