Chronic lymphocytic leukaemia of the B-cell type (B-CLL) is a disease characterized by expansion of mature-appearing B-lymphocytes in the peripheral blood and bone marrow ( Dighiero et al, 1991 ). The malignant monoclonal B cells display several phenotypic and functional differences compared with their normal cellular counterparts (reviewed by Zaknoen & Kay, 1990). B-CLL cells typically express low-density surface membrane immunoglobin, mostly IgM or IgD or both and a single κ or λ light-chain. Accepted requirements for diagnosis also include a specific immunophenotype, absolute lymphocytosis and infiltration of the bone marrow by lymphocytes ( Bennet et al, 1989 ; Matutes et al, 1994 ). Although the aetiology and pathogenesis of the disease is still in many respects unknown, recent data have provided important information about factors related to disease progression and cellular mechanisms involved in the leukaemic process. The lack of spontaneous in vitro proliferation of malignant B cells supports the theory that expansion of the monoclonal B-cell population is largely dependent on exogenous growth stimulation provided by environmental cells and autocrine growth factors ( Collins et al, 1989 ). Cytokines such as TNF-α, interleukin-1β (IL-1β), IL-2, IL-4, IL-6, IL-8, IL-10 and interferon-α have been proposed to play a role in the regulation of growth and death of leukaemic B cells ( Aderka et al, 1993 ; Buschle et al, 1993 ; Dancescu et al, 1992 ; Di Celle et al, 1994 ; Fluckiger et al, 1994 ; Larsson et al, 1993 ; Panayiotides et al, 1994 ; Van Kooten et al, 1992 ). In some studies, B cells have also been shown to express functional receptors for some of these cytokines, such as TNF-α, IL-6 and IL-2, suggesting the existence of possible autocrine cytokine loops ( Cordingley et al, 1988 ; Fluckiger et al, 1993 ; Lavabre-Bertrand et al, 1995 ). Exogenously administered TNF may also show a co-stimulatory effect on mitogen-activated normal human B cells as well as providing a proliferative signal to leukaemic B cells in B-CLL ( Digel et al, 1989 ). Recent reports emphasize the role of TNF-α as an autocrine and paracrine growth factor for B-CLL cells and the role of IL-6 as an inhibitory factor for this TNF-α-induced proliferation ( Reittie et al, 1996 ). Some reports suggest that there is constitutive spontaneous expression of IL-6 and TNF-α in CLL cells of B-CLL patients, the mechanism and meaning of which are still unknown ( Biondi et al, 1989 ; Foa et al, 1990 ). The present study was designed to investigate interleukin-6 and TNF-α production in B-CLL cells from patients at different stages of disease, in order to determine possible connections between these cytokines and disease aggressiveness, and prognostic parameters.