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Expression of HLA Class II (DR, DQ) Determinants by Normal and Chronic Myeloid Leukemia Granulocyte/Monocyte Progenitors¹

Clinica Medica A ed Istituto di Genetica Medica-Universita' di Torino, Centro di Immunogenetica ed Istocompatibilita', CNR Torino, and Divisione di Medicina Generale E, Sezione di Ematologia, Ospedale S. Giovanni Battista e della Citta' di Torino, Torino, Italy

It has been suggested that the expression of certain HLA class II antigens stemming from three distinct loci (DR, DP, and DQ) is important not only in the regulation of the immune response but also on the response of hemopoietic precursors to factors inhibiting myelopoiesis. Changes in the expression of DR antigens may be involved in the pathogenesis of altered cell proliferation in chronic myeloid leukemia, since they result in decreased sensitivity of the colony forming units, granulocyte-macrophage to prostaglandin E and acidic isoferritins. In studies using monoclonal antibodies against monomorphic DR or DQ determinants, in a complement-dependent cytotoxic assay, it was found that nearly all normal and chronic myeloid leukemia bone marrow colony forming units, granulocyte-macrophage express DR antigens. The dose response curve was similar for both normal and leukemic precursors. Leukemic peripheral blood precursors were more sensitive than were normal peripheral blood precursors. Normal colony forming units, granulocyte-macrophage did not express DQ antigens, whereas these were expressed in varying quantities by leukemic cells. This study shows that, in the patients we studied, leukemic cells express DR antigens in amounts comparable to normal. In addition, varying amounts of DQ antigens may be observed on leukemic but not on normal progenitors, perhaps as a consequence of an increase in the number of antigens also expressed by normal cells, though in an amount below the detection threshold of cytotoxicity techniques.

¹ This work was supported by grants from CNR, Progetti Finalizzati "Oncologia," and "Ingegneria Genetica e Basi Molecolari delle Malattie Ereditarie" and by "Associazione Italiana per la Ricerca sul Cancro."

Received 5/30/85. Revised 10/30/85. Accepted 12/26/85.