Abstract
Clinical optimism for dendritic cell vaccination against ovarian cancer has been tempered by the knowledge that tumors avail themselves of multiple mechanisms of immune evasion, thus blunting the efficacy of therapeutic vaccination. Mechanisms of immune suppression include infiltration by regulatory T cells (Treg) and myeloid suppressor cell populations, expression of co-inhibitory receptors, and expression of indoleamine 2,3-dioxygenase (IDO). Expression of both B7-H1 and IDO are associated with differentiation and recruitment of Treg, and clinical studies have shown that each of these mechanisms correlates independently with increased morbidity and mortality in ovarian cancer patients. In sharp contrast, recent studies have indicated that Th17 cell infiltration in ovarian cancer correlates with improved patient outcomes and prolonged overall survival. Given that IDO plays a pivotal role in the balance between Treg and Th17 immunity, elucidation of the mechanisms that regulate IDO activity and immune suppression may lead to novel adjuvants to boost the clinical efficacy of dendritic cell vaccination against ovarian cancer and other malignancies.
Highlights
THE CLINICAL PROBLEM Clinical studies have shown that the immune system plays an active and possible critical role in the pathogenesis of ovarian cancer, disease progression, and overall survival
In sharp contrast with the evidence that Treg infiltration is associated with poor outcomes in ovarian cancer, Th17 T cell infiltration correlates with more favorable clinical outcomes [13]
Elucidation of the multiple facets of immune regulation in the ovarian tumor micro-environment has sharpened the appreciation that there are formidable barriers to therapeutic dendritic cell (DC) vaccination, but has raised the prospect for mechanism-based interventions
Summary
THE CLINICAL PROBLEM Clinical studies have shown that the immune system plays an active and possible critical role in the pathogenesis of ovarian cancer, disease progression, and overall survival. Expression of both B7-H1 and IDO are associated with differentiation and recruitment of Treg [7,8,9], and clinical studies have shown that each of these mechanisms correlates independently with increased morbidity and mortality in ovarian cancer patients [10,11,12].
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