Hypothesis for a mechanism behind the accelerated development of AIHA in CD47^−/− NOD mice.

At low levels of anti-RBC autoantibodies (1) inhibitory CD47-SIRPα signaling prevents erythrophagocytosis in CD47⁺ NOD mice, whereas the absence of CD47-SIRPα signaling in CD47^−/−NOD mice results in erythrophagocytosis (2).15 This may result in increased antigen presentation of self RBC peptides and sustained autoantibody production, which through increased RBC opsonization will lead to accelerated erythrophagocytosis and progressive exacerbation of AIHA in CD47^−/− NOD mice (3).