학술논문

Tumor-associated B7-H1 promotes T-cell apoptosis: A potential mechanism of immune evasion.
Document Type
Article
Source
Nature Medicine. Aug2002, Vol. 8 Issue 8, p793. 8p.
Subject
*T cells
*APOPTOSIS
*MONOCLONAL antibodies
*CELL lines
*BREAST cancer
Language
ISSN
1078-8956
Abstract
B7-H1, a recently described member of the B7 family of costimulatory molecules, is thought to be involved in the regulation of cellular and humoral immune responses through the PD-1 receptor on activated T and B cells. We report here that, except for cells of the macrophage lineage, normal human tissues do not express B7-H1. In contrast, B7-H1 is abundant in human carcinomas of lung, ovary and colon and in melanomas. The pro-inflammatory cytokine interferon-γ upregulates B7-H1 on the surface of tumor cell lines. Cancer cell?associated B7-H1 increases apoptosis of antigen-specific human T-cell clones in vitro, and the apoptotic effect of B7-H1 is mediated largely by one or more receptors other than PD-1. In addition, expression of B7-H1 on mouse P815 tumor increases apoptosis of activated tumor-reactive T cells and promotes the growth of highly immunogenic B7-1+ tumors in vivo. These findings have implications for the design of T cell?based cancer immunotherapy. [ABSTRACT FROM AUTHOR]