ANTERIOR CHAMBER INFLUENCE ON OCULAR ANTIGENS
前房对眼抗原的影响
基本信息
- 批准号:6130964
- 负责人:
- 金额:$ 33.49万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1993
- 资助国家:美国
- 起止时间:1993-11-01 至 2004-06-30
- 项目状态:已结题
- 来源:
- 关键词:B lymphocyte T cell receptor T lymphocyte anterior chamber antigen presenting cell antigens cellular immunity cytokine cytotoxic T lymphocyte delayed hypersensitivity enzyme linked immunosorbent assay eye injury genetically modified animals immunity immunopathology immunosuppression inflammation laboratory mouse mixed tissue /cell culture polymerase chain reaction trauma western blottings
项目摘要
DESCRIPTION (Adapted from applicant's abstract): Systemic immune responses to
anterior chamber antigens are deviant in that certain types of immune effectors
(delayed hypersensitivity and complement-fixing antibodies) are selectively
suppressed, whereas other effectors (cytotoxic T cells, non-complement fixing
antibodies) are retained. This pattern of response has been termed Anterior
Chamber Associated Immune Deviation (ACAID). The mechanisms of this phenomenon
involve shaping of the initial response to ocular antigens by the ocular
microenvironment, so that regulatory cells arise that dictate the type of
response generated. If the eye is altered by inflammation, trauma or disease,
its capacity to promote ACAID is abolished. The experimental plan proposed
addresses 3 related hypotheses, while making use of ovalbumin T cell receptor
(OVA TCR) transgenic mice: (i) that OVA-specific TCR transgenic T cells,
activated in vitro by OVA-pulsed TGF-beta2-treated antigen presenting cells
(APC), become regulatory T cells that suppress, respectively, the induction and
expression of delayed hypersensitivity in vivo; (ii) that pigment epithelium
inhibits activation of Th1-type cells and converts activated T cells into
regulatory cells; and (iii) that immune privilege and ACAID are abolished
acutely in ocular inflammation, but secondary mechanisms intervene to restore
immune suppression and ACAID. These hypotheses give rise to 3 specific aims:
(1) to characterize and describe mode of action of regulatory T cells of ACAID;
(2) to describe mode of action of ocular factors that promote immune privilege
and ACAID in normal eyes; and (3) to determine the consequences of inflammation
and trauma on ocular immune privilege.
The investigators contend that the experimental plan will provide key
information concerning the molecular basis of ocular immune privilege and ACAID
in the normal mouse, and will reveal molecular processes that abolish immune
privilege and allow it to be restored. A secondary benefit will be a
significant expansion of knowledge of genes that are differentially regulated
in the cellular processes by which ACAID is induced and expressed. The
anticipation is that new knowledge concerning key genes in ACAID and immune
privilege will lead to therapeutic strategies directed at alleviating ocular
inflammatory disease and promoting orthotopic graft acceptance.
描述(改编自申请人的摘要):系统免疫反应
前房抗原的异常之处在于某些类型的免疫效应物
(迟发性超敏反应和补体固定抗体)是选择性的
被抑制,而其他效应器(细胞毒性 T 细胞、非补体固定
抗体)被保留。这种反应模式被称为前向反应
室相关免疫偏差(ACAID)。这种现象的发生机制
涉及眼部对眼部抗原的初始反应的形成
微环境,因此调节细胞的出现决定了
生成响应。如果眼睛因炎症、外伤或疾病而改变,
其促进 ACAID 的能力被取消。提出的实验方案
利用卵清蛋白 T 细胞受体解决 3 个相关假设
(OVA TCR) 转基因小鼠:(i) OVA 特异性 TCR 转基因 T 细胞,
在体外被 OVA 脉冲的 TGF-β2 处理的抗原呈递细胞激活
(APC),成为调节性 T 细胞,分别抑制诱导和
体内迟发型超敏反应的表达; (ii) 色素上皮
抑制 Th1 型细胞的活化并将活化的 T 细胞转化为
调节细胞; (iii) 废除免疫特权和 ACAID
眼部炎症严重,但次要机制干预以恢复
免疫抑制和 ACAID。这些假设产生了 3 个具体目标:
(1) 表征和描述 ACAID 调节性 T 细胞的作用模式;
(2) 描述促进免疫豁免的眼部因素的作用方式
正常眼中的 ACAID; (3) 确定炎症的后果
和创伤对眼部免疫特权的影响。
研究人员认为,实验计划将提供关键
有关眼部免疫豁免和 ACAID 的分子基础的信息
在正常小鼠中,并将揭示消除免疫的分子过程
特权并允许其恢复。次要好处是
显着扩展差异调节基因的知识
在诱导和表达 ACAID 的细胞过程中。这
预期关于 ACAID 和免疫关键基因的新知识
特权将导致针对缓解眼部疾病的治疗策略
炎症性疾病和促进原位移植物接受。
项目成果
期刊论文数量(0)
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会议论文数量(0)
专利数量(0)
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J WAYNE STREILEIN其他文献
J WAYNE STREILEIN的其他文献
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{{ truncateString('J WAYNE STREILEIN', 18)}}的其他基金
AUTOIMMUNITY ASSOCIATED WITH PIGMENT DISPERSION GLAUCOMA
与色素分散性青光眼相关的自身免疫
- 批准号:
6598293 - 财政年份:2003
- 资助金额:
$ 33.49万 - 项目类别:
ASSAY FOR HAPTEN SPECIFIC PRIMING OF T LYMPHOCYTES
T 淋巴细胞半抗原特异性启动的测定
- 批准号:
6141416 - 财政年份:1998
- 资助金额:
$ 33.49万 - 项目类别:
Training Program in the Molecular Bases of Eye Disease
眼病分子基础培训计划
- 批准号:
6314342 - 财政年份:1997
- 资助金额:
$ 33.49万 - 项目类别:
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