Autoimmune aspects of aplastic anemia

Recovery of bone marrow function in aplastic anemia patients treated with immunosuppressive therapy first suggested a role for the immune system in bone marrow failure. High recovery rates in patients treated with immunosuppressive therapy suggested that an immune mechanism may be a final common pathway of marrow failure in this disease. In vitro studies have shown that aplastic peripheral blood and marrow cells and their supernatants are capable of suppressing hematopoiesis by autologous and normal marrow. Soluble factors identified in this system include gamma interferon and lymphotoxin. The interaction of these molecules with positive growth factors, the role of synergy with other negative regulators, and their role in the pathogenesis of bone marrow failure are discussed. Lymphokine and lymphocyte abnormalities in aplastic anemia may be manifestations of an underlying viral etiology. Three examples are discussed: Epstein-Barr virus-associated aplastic anemia; B19 parvovirus bone marrow failure; and HIV-induced neutropenia.