B7-homolog 1 expression by human glioma: a new mechanism of immune evasion

Abstract

Immunosuppressive soluble factors such as transforming growth factor beta and cell surface molecules such as FasL may contribute to the immune evasion of malignant glioma. B7 homolog 1 is a member of the B7 family of costimulatory molecules implicated in the negative regulation of T cell immune responses. Here, we show that human glioma cell lines express B7 homolog 1 protein that reduces interferon-gamma production by activated T cells. The expression of B7 homolog 1 in vivo was demonstrated in a large series of human glioma samples, with a significant correlation between the level of B7 homolog 1 expression and the tumor grade. Overall, our data suggest that B7 homolog 1 may be involved in the immune evasion of glioma and encourage the blockade of this pathway in future immunotherapies.