[Role of myeloid cell abnormalities in the pathogenesis of aplastic anemia:a review of research advances].

Aplastic anemia is a disorder characterized by bone marrow failure and peripheral pancytopenia. T cell-mediated injury to hematopoietic stem and progenitor cells (HSPCs) is recognized as a key immunological mechanism underlying its pathogenesis. Recent evidence indicates that myeloid cell abnormalities also contribute to the bone marrow immunopathology of aplastic anemia. Myeloid populations-including dendritic cells, mononuclear phagocytes, myeloid-derived suppressor cells, and mast cells-may disrupt the local bone marrow immune and hematopoietic microenvironment through their involvement in antigen presentation, immunosuppression, inflammation resolution, efferocytosis, and stromal support. Such abnormalities may not only sustain aberrant T cell responses and impair hematopoietic support, but also correlate with disease relapse and clonal evolution. This review summarizes current understanding of the role of myeloid cell abnormalities in the pathogenesis of aplastic anemia, aiming to provide a reference for further elucidation of its immune mechanisms and disease progression.