LIVER TRANSPLANTATION--THE ROLE OF DENDRITIC CELLS

肝移植——树突状细胞的作用

• 批准号: 2905746
• 负责人: Angus W Thomson
• 金额: $ 18.3万
• 依托单位: UNIVERSITY OF PITTSBURGH AT PITTSBURGH
• 依托单位国家: 美国
• 财政年份: 1996
• 资助国家: 美国
• 起止时间: 1996-05-01 至 2000-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2905746
• 关键词: MHC class II antigen; anergy; antibody; apoptosis; cadherins; cytokine; cytokine receptors; cytotoxic T lymphocyte; dendritic cells; extracellular matrix proteins; gene expression; heart transplantation; homologous transplantation; immune tolerance /unresponsiveness; immunoglobulins; immunosuppression; integrins; laboratory mouse; liver transplantation; phenotype; polymerase chain reaction; receptor binding; selectins; skin transplantation; transplantation immunology

DESCRIPTION: (Adapted from the applicant's abstract) It is noted that the orthotopic liver transplant model in mice results in virtually 100 percent tolerance and survival of recipients without need for immunosuppression and also results in transfer of dendritic cells systemically within the recipient. Progenitor dendritic cells are deficient in MHC Class II and stimulatory molecule expression and allostimulatory activity and can also prolong allograft survival in certain circumstances. These immunosuppressive properties of progenitor dendritic cells are controlled by both cytokines and by matrix interactions. Therefore the applicant hypothesizes that regulation of the expression of cell surface MHC antigens and T cell costimulatory molecules on dendritic cells determines their potential to induce tolerance and immunity. Three specific aims are proposed: I. Determine how cytokines and matrix proteins alter the phenotype and function of liver dendritic cells. II. Define the cellular and molecular mechanisms by which alterations in dendritic cell phenotype and function alter T cell responses in vitro. III. Establish the in vivo relevance of alterations in dendritic cell expression of co-stimulatory molecules by extending their observation that dendritic progenitors promote the survival of organ allografts.

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