Molecular mechanisms of autoimmune hemolytic anemia

Abstract Autoimmune hemolytic anemia (AIHA) is an acquired immunological disease in which red blood cells (RBCs) are selectively attacked and destroyed (hemolyzed) by autoantibodies produced by the patient's own immune system. Several hypotheses regarding the mechanisms underlying the development of AIHA have been proposed, but the actual pathogenesis remains unclear. Since the major autoantigens in warm AIHA were determined to be Rh protein, band 3 and glycophorin A in 1993, helper T cells (Th1, Th2 and Th17) and regulatory T (Treg) cells specifically reacting to Rh peptides were reported in patients with AIHA. Recently, Th1 responses were found to be suppressed with synthetic peptides that are recognized by the Treg cells, and Th17 cells and interleukin 17 were shown to contribute to the induction and the development of AIHA. This approach to understanding AIHA pathogenesis may provide clues to finding novel targets for immunotherapy against AIHA.