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Detection of Both T-Cell and Ia-like Antigens on Cells from Patients with Acute Myelomonocytic Leukemia and Chronic Myelogenous Leukemia in Blast Crisis¹

Departments of Microbiology and Immunology [J. K. A., R. S. M.] and Medicine [J. O. M.], Duke University Medical Center, Durham, North Carolina 27710

Appropriately absorbed antisera to the lymphoblastoid cell lines HSB and SB detect a human T-lymphocyte-associated antigen (TLAA) and the human Ia-like antigens, respectively. Cells from some patients with acute myelomonocytic leukemia (AMML) and chronic myelogenous leukemia in blast crisis expressed both TLAA and la antigens when tested in a complement-dependent microcytotoxicity assay (>90% lysis with both antisera). When patients were in remission, expression of TLAA and la antigens returned to normal values. Quantitative absorption of anti-TLAA serum with increasing numbers of AMML cells showed that these cells could remove reactivity of the serum for both HSB and human thymocytes. Similarly, absorption of anti-la serum with AMML cells removed all serological reactivity when this serum was tested on chronic lymphocytic leukemia cells or normal B-cells. These serological findings were confirmed by immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis studies using radiolabeled antigens. Cells from an AMML patient were labeled with ¹²⁵I using lactoperoxidase; both the TLAA and la antigens were precipitated from the resulting solubilized membrane preparation. Leukemic cells from one AMML patient and one patient with chronic myelogenous leukemia in blast crisis were studied for la and TLAA antigens with a double fluorescence technique. Over 80% of the cells showed dual fluorescence.

¹ Supported by USPHS Grants CA 08975 and CA 11265 from the National Cancer Institute and Grant AM 08054 from the National Institute of Arthritis, Metabolism, and Digestive Diseases.

² To whom requests for reprints should be addressed, at Box 3839, Duke University Medical Center, Durham, N. C. 27710.

Received 4/30/79. Accepted 8/29/79.