title: Role of accessory cells in cytokine production by T cells in chronic B-cell lymphocytic leukemia.
abstract: We investigated the production of cytokines by highly purified T helper cells from B-cell chronic lymphocytic leukemia (B-CLL) patients stimulated by different activation pathways, and we studied the influence of various accessory cell populations on the pattern of the secretion of cytokines, including interleukin (IL)-2, IL-4, interferon-gamma (IFN-gamma), and IL-10. Neither a qualitative nor a quantitative difference in cytokine production and proliferative capacity was observed in CLL-derived purified T cells compared with normal individuals, when T cells were stimulated by different pathways, including CD3, CD2, and costimulation with CD28. Addition of autologous accessory cells (aAC), however, dramatically influenced the cytokine pattern of normal versus B-CLL-derived T cells. CLL cells as aAC caused a marked increase of IL-2, whereas IFN-gamma was only slightly induced and IL-4 was not influenced. In contrast, in normal individuals addition of aAC, which predominantly consisted of monocytes, resulted in a significant increase of IFN-gamma and a reduction of IL-4 secretion. IL-2 production was inhibited by higher concentrations of aAC. The increased stimulation of IL-2 production by CLL cells was not specific to the leukemic cell population, as purified B cells from normal individuals had the same effect. On the other hand, purified monocytes from CLL patients and controls both induced IFN-gamma production and inhibited IL-4 secretion. After antigen-specific stimulation with tetanus toxoid, cytokine secretion was influenced by the type of aAC in a similar pattern. We conclude that T helper cells derived from patients with B-CLL are intrinsically normal and that the predominance of B cells as accessory cells in CLL significantly alters the immune function of T helper cells in vitro.
authors.affiliation: Third Department of Internal Medicine, Johannes Gutenberg University School of Medicine, Mainz, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Decker
authors.forename: T
authors.initials: T
authors.lastname: Flohr
authors.forename: P
authors.initials: P
authors.lastname: Trautmann
authors.forename: M J
authors.initials: MJ
authors.lastname: Aman
authors.forename: W
authors.initials: W
authors.lastname: Holter
authors.forename: O
authors.initials: O
authors.lastname: Majdic
authors.forename: C
authors.initials: C
authors.lastname: Huber
authors.forename: C
authors.initials: C
authors.lastname: Peschel
mesh_terms: D000938:Antigen-Presenting Cells / Q000502:physiology*; D001402:B-Lymphocytes / Q000502:physiology; D018801:CD2 Antigens / Q000502:physiology; D017252:CD3 Complex / Q000502:physiology; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism*; D016207:Cytokines / Q000096:biosynthesis*; D006801:Humans; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000503:physiopathology*; D008213:Lymphocyte Activation; D008211:Lymphocyte Cooperation; D009000:Monocytes / Q000276:immunology; D015398:Signal Transduction; D013745:Tetanus Toxoid / Q000276:immunology
chemical_list: D018801:CD2 Antigens; D017252:CD3 Complex; D016207:Cytokines; D013745:Tetanus Toxoid