Immunoregulation was assessed in a group of patients with myelodysplasia (MDS) by flow cytometric analysis of peripheral blood lymphocyte subsets and in vitro studies of mitogen-stimulated T-lymphocyte blastogenesis. Mitogenesis was significantly depressed in MDS patients compared to controls (p less than .001) and a similar defect was found in a small group of patients with untreated acute nonlymphocytic leukemia (ANLL) (p less than .005). The impaired mitogenic response ability of T-cells in these patients did not appear to be the result of alteration in lymphocyte subpopulation ratios. The observed defect might result from defective cooperation between T-lymphocytes and abnormal myeloid elements. Alternatively, the lymphocytes themselves could be derived from the abnormal clone and thus be functionally abnormal.

A panel of monoclonal antibodies recognizing myeloid cell surface differentiation-associated antigens was used to study the peripheral blood myeloid population of 23 patients with myelodysplastic syndromes (MDS) and 23 controls. A marker for immaturity, defined by the presence of the antigen recognized by the My9 antibody, was found to persist on the surface of mature neutrophils in a subgroup of MDS patients. Abnormal My9 positivity was concentrated primarily, but not exclusively, in previously described morphologically defined subgroups of MDS patients considered to be at highest risk for leukemic conversion. Longitudinal study of a larger number of patients will be required to test the hypothesis that abnormal persistence of My9 may have prognostic significance.

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The development of a large cell lymphoma in a patient with chronic lymphocytic leukemia (Richter syndrome) is associated with a poor prognosis. There is dispute regarding the clonal origin of the large cell component. We described a patient in whom prolonged remission of the large cell component was achieved with combination chemotherapy, followed by subsequent reemergence of the less aggressive CLL clone. Serial cell surface phenotypic data are presented suggesting origin of both histologies from a common B-cell clone.