The humoral antibody immunodeficiency in two patients with T-cell chronic lymphocytic leukemia (T-CLL) appeared to be the result of immunoregulatory abnormalities in the leukemic T-cell populations. Both patients had CD4-t CD45RS "virgin" or suppressor-inducer T-CLL, but Patient 1 had hypogammaglobulinemia and Patient 2, immunoglobulin (Ig) M hypergammaglobulinemia. Although, CD25+ interleukin-2 (IL-2) receptors were present on leukemic T-cells of both patient, OKT9-t (CD71) transferrin receptors and OKTlO (CD38) activation antigens were found only on Patient 2's cells. Highly elevated amounts of IL-2 was secreted from phytohemagglutinin-stimulated and concanavalin A-stimulated T-celis in both patients. In Patient 1 with hypogammaglobulinemia, immune defects involve Tcells, first an intense suppressor activity on B-cell-induced IgM and IgG synthesis and, second, deficient production of B-cell growth factor (BCGF) and B-cell differentiation factor (BCDF). In Patient 2, highly elevated BCGF and IgM-specific BCDF was secreted by T-cells, a mechanism leading to IgM hypergammaglobulinemia in this patient. These studies stress the importance of BCGF and BCDF activity of leukemic T-cells in humoral antibody immunodeficiency disorders in T-CLL cases. Cancer 67:2518-2522.1991.
UMORAL IMMUNODEFICIENCY DISORDERS may be H attributable to various defects in the development and function of the immune system.'-3 Recently, the Tcell-derived lymphokines, such as interleukin-2 (IL-2), Bcell growth factor (BCGF), and B-cell differentiation factor (BCDF) with specific effects on immune regulation of Bcell proliferation and differentiation, have been identified.4*' There are several immune reactions where control of the lymphokine-related response could have a clinical effect.' Therefore, in vitro assessment of lymphocyte function and lymphokine secretion is crucial in the analysis of the pathogenesis of several diseases involving immune dysfunction and immunodeficiency.