• 1 January 1985
    • journal article
    • research article
    • Vol. 66  (3) , 533-541
Abstract
To define further the role of marrow T suppressor lymphocytes in the pathogenesis of the hypoproliferative anemia in all Rai clinical stages of B cell chronic lymphocytic leukemia (CLL), marrow erythroid progenitor cell (CFU-E and BFU-E) frequency, marrow T.gamma. lymphocyte frequency per 1,000 nucleated marrow cells, and T cell-erythroid progenitor cell interactions were examined in 30 CLL patients and normal control subjects. As compared with control subjects, decreased numbers of CFU-E and BFU-E were found in patient marrow depleted of neoplastic B cells in all Rai stages of the disease. As a group, Rai stage III through IV patients with or without aplasia (CLL-aplasia) had significantly fewer CFU-E and BFU-E than did Rai 0 through II stage patients. The numbers of T.gamma. cells infiltrating CLL marrows were increased 3, 9, and 20 times normal in Rai 0 through II, Rai III through IV, and CLL-aplasia groups, respectively. Removal of T cells from marrow increased growth in CFU-E and BFU-E in all Rai 0 through IV patients, but the increase was significant in the CLL-aplasia group only (P < .05). However, autologous co-culture of marrow T cells or T.gamma. cells but not B cells with marrow B + T-depleted null cells at ratios of 0.2:1 to 1:1 suppressed CFU-E and BFU-E growth in all three patient groups. We conclude that the hypoproliferative anemia occurring in the course of B cell CLL is due to gradual accumulation in the marrow of T.gamma. lymphocytes which suppress erythroid progenitor cell growth. T.gamma. cell suppression of erythopoiesis and marrow T.gamma. cell expansion is detectable in the earliest Rai stages of the disease.