Introduction

Although aplastic anemia (AA) is a syndrome of unknown etiology as defined by the clinical picture, a large body of evidence suggests that T-cells have an important role in its development (Nakao, 1997: 127; Young, 1994: 68; 1996: 55). High remission rates in recent clinical trials using a combination of immunosuppressive drugs such as antithymocyte globulin (ATG) and cyclosporin have strengthened the notion that AA is a T-cell disease rather than a stem-cell disease (Bacigalupo et al., 1995: 1348; Frickhofen et al., 1991: 1297; Rosenfeld et al., 1995: 3058). Understanding the immunological abnormalities in individual patients is important in choosing an appropriate therapy; although a >80% rate of response to immunosuppressive therapy is anticipated, some patients may need allogeneic stem-cell transplantation because of nonimmunological pathogenesis, such as drug toxicities or intrinsic stem-cell defects. Moreover, accumulation of patients' data obtained using classic or novel immunological methods would be useful in identifying the inciting events of AA that remain totally unknown.

Immunophenotyping data on T-cells and natural killer cells in bone marrow and peripheral blood

The immune response to foreign antigens or ‘self’ antigens is usually associated with changes in the T-cell subsets defined by immunophenotype. In AA, where certain antigens probably incite the immune attack against hemopoietic progenitor cells, an imbalance between different T-cell subpopulations in the bone marrow or peripheral blood has been suspected.