Abstract
Immune evasion is an important hallmark of cancer, and a better understanding of this mechanism is essential for the development of effective strategies against cancer. The B7 homolog 1 (B7-H1)/programmed cell death 1 (PD-1) pathway has been demonstrated as a major mechanism of immune evasion in tumor site, and its blockade therapy shows very encouraging results in clinical trials. Inducible B7-H1 expression in tumor microenvironment is complex, with multidimensional interactions and expression by different subsets of hematopoietic and nonhematopoietic cells. Understanding these interactions and how tumors take advantage of this pathway can help us design future strategies for better therapeutic efficacy and to overcome resistances.