A model showing the possible duality in roles of a single autoreactive B cell during the regulation or promotion of autoimmunity. Self antigen recognition by an autoreactive B cell receptor leads to activation of a killer/regulatory or stimulatory B cell depending on the secondary signals received concurrently. LPS and factors promoting a Th2 effector phenotype may favor production of killer/regulatory B cells, while factors that promote a Th1 or Th17 phenotype may favor a stimulatory B cell phenotype. Killer/regulatory B cells producing IL-10, TGFβ, FasL, and/or other death-inducing ligands may interact with an autoreactive T cell leading to induction of tolerance. Stimulatory B cells producing IL-6, TGFβ, upregulated B7 molecules, and/or decreased death ligand expression may interact with autoreactive T cells leading to induction of IL-17 and promotion of autoimmunity. It remains unclear whether a single autoreactive B cell can be forced into either one of these roles, or whether regulatory and stimulatory autoreactive B cells come from separate B cell compartments