Update on checkpoint blockade therapy for XXXX .

@entity4634 @entity1733 @entity706 @entity5 @entity8395 @entity1893 @entity4386
Although @entity5 cells express antigens recognizable to the immune system, @entity5 employ a number of diverse mechanisms aimed at subverting the host anti- @entity5 immune response. Tumor immune evasion pathways have been most thoroughly studied in solid @entity5 . However, emerging data has demonstrated that @entity5 of hematopoietic origin are also able to co-opt their local environment in order to escape immune attack. Activated T cells upregulate negative costimulatory receptors, such as @entity8395 ( @entity8395 ) and @entity4386 ( @entity4386 ). Engagement of @entity8395 or @entity4386 with ligands expressed on @entity5 cells or professional antigen presenting cells results in down-regulation of effector T cell function and represents a potent mechanism of immune evasion across a number of human @entity5 . Antibodies which block @entity8395 / @entity4634 interactions have demonstrated remarkable activity in a number of solid @entity5 subtypes. Interestingly, recent data have demonstrated that in select subtypes of Hodgkin ( @entity1733 ) and @entity1893 ( @entity1893 ), the @entity8395 ligands are over-expressed due to a genetic amplification of the loci encoding them. Other mechanisms of @entity4634 over-expression in @entity706 have also been elucidated. Reports from early-phase clinical trials of @entity8395 blockade have demonstrated remarkable effectiveness in @entity1733 , and also appear active against some NHLs. We review the mechanisms of @entity4634 expression in @entity706 and also the early results of anti- @entity8395 therapy in this disease.
