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lüll Pathophysiologic mechanisms in acquired aplastic anemia Young NSHematology Am Soc Hematol Educ Program 2006[]; ä (ä): 72-7Aplastic anemia, an unusual hematologic disease, is the paradigm of the human bone marrow failure syndromes. Absence of hematopoietic cells has been recognized from the characteristic morphology for a century; an immune pathophysiology has been inferred from improvement in blood counts with immunosuppressive therapy in the majority of patients. Molecular mechanisms underlying both T cell effector cells and the target marrow stem and progenitor cells are now being identified. Activated type 1 cytotoxic T cells and type 1 cytokines have been implicated in cell culture experiments; clues to the molecular basis of the aberrant immune response include cytokine gene polymorphisms and abnormalities in the regulatory pathways for gamma-interferon. For stem cell depletion, mutations in genes of the telomere repair complex are present in some patients with apparently acquired aplastic anemia. Telomerase deficiency is associated with short telomeres and a quantitative reduction in marrow progenitors and likely also a qualitative deficiency in the repair capacity of hematopoietic tissue.|Anemia, Aplastic/*etiology/immunology/pathology[MESH]|Cytokines/genetics[MESH]|Hematopoietic Stem Cells/pathology[MESH]|Humans[MESH]|Mutation[MESH]|Polymorphism, Genetic[MESH]|T-Lymphocytes[MESH]|Telomerase/deficiency[MESH] |