TSHR and Graves disease: The role of B cells in Graves’ hyperthyroidism is well established, not only in their capacity as immunoglobulin-secreting plasma cells producing the pathogenic TRAb autoantibody, but also in their ability to act as antigen-presenting cells, likely presenting TSHR epitopes to T cells to perpetuate disease, as well as modulating the immune response by producing both pro- and anti-inflammatory cytokines and chemokines (13).