Advances in understanding of the immune microenvironment have highlighted the 
role of immunosuppressive T cell, myeloid, dendritic and monocytic 
sub-populations in inhibition of the anti-tumor immune response. The role of B 
cells in modulating the immune response to solid tumors as well as lymphoid 
malignancies is less well understood. Murine models of autoimmune disease have 
defined B regulatory cell (Breg) subsets with immune suppressive activity, 
including B cell subsets that express IL-10, and transforming growth factor-β, 
which can facilitate T regulatory cell recruitment and expansion. Multiple 
murine tumor models point to the existence of similar immune suppressive B cell 
sub-populations that can migrate into tumor deposits and acquire an immune 
suppressive phenotype, which then leads to attenuation of the local anti-tumor 
immune response. Other murine models of viral or chemically induced skin 
carcinogenesis have identified a pivotal role for B cells in promoting 
inflammation and carcinogenesis. While many human solid tumors demonstrate 
significant B cell infiltration and/or tertiary lymphoid structure formation, 
the functional properties of tumor-infiltrating B cells and their effects on 
immunity are poorly understood. Recent successes in early Phase I/II trials 
using anti-checkpoint inhibitor antibodies such as nivolumab or pidilizumab 
directed against PD-1 in the setting of Hodgkin's and non-Hodgkin's lymphomas 
validate the therapeutic utility of reversing B cell-mediated immune 
suppression. Further studies to define Breg subsets, and mechanisms of 
suppression, may provide new avenues for modulation of the immune response and 
meaningful therapeutic intervention in both lymphoid and solid tumors.