title: Defective IL-2 receptor expression in lymphocytes of patients with arsenic-induced Bowen's disease.
abstract: The immune function of peripheral mononuclear cells (MNC) in patients with endemic arsenic-induced Bowen's disease (BD) was investigated. Many cytokines and immune-related factors were determined in the present study. Interleukin-1beta and TNF-alpha production was used as an indicator of monocyte/macrophage function. II-2 and sIL-2R production was used as an indicator of lymphocyte activation. The release of sCD4 and sCD8 was used as an indicator of activation of respective T-cell subpopulations. Production of IFN-gamma and IL-2 reflected the cellular effector function of helper T-cells type 1. In vivo cell-mediated immunity was also assessed by estimation of the percentage of T-cells in peripheral blood MNC and the nonspecific delayed-type hypersensitivity (DTH) response to 2,4-dinitrochlorobenzene (DNCB). Both assays revealed depressed cell-mediated immunity in BD. Compared with healthy controls, spontaneous and PHA-induced IFN-gamma and TNF-alpha production was significantly decreased in BD whereas spontaneous release of IL-2, sCD4 and sCD8 was significantly increased. Although PHA stimulation increased IL-2 release, the expression of IL-2R alpha and beta chains and the release of sIL-2R were not proportionately increased in BD. In addition, IL-2-mediated [3H]-thymidine incorporation by MNC in patients with BD was significantly decreased. These findings suggest that the defective cell-mediated immune function in BD is due to impairment of membrane IL-2R expression in lymphocytes after stimulation.
authors.affiliation: Department of Dermatology, Kaohsiung Medical College, Taiwan, Republic of China. dermyu@cc.kmc.edu.tw
authors.forename: H S
authors.initials: HS
authors.lastname: Yu
authors.forename: K L
authors.initials: KL
authors.lastname: Chang
authors.forename: C L
authors.initials: CL
authors.lastname: Yu
authors.forename: C S
authors.initials: CS
authors.lastname: Wu
authors.forename: G S
authors.initials: GS
authors.lastname: Chen
authors.forename: J C
authors.initials: JC
authors.lastname: Ho
mesh_terms: D000368:Aged; D001151:Arsenic / Q000009:adverse effects*; D001913:Bowen's Disease / Q000139:chemically induced / Q000276:immunology*; D015704:CD4 Antigens / Q000096:biosynthesis; D016827:CD8 Antigens / Q000096:biosynthesis; D006801:Humans; D006968:Hypersensitivity, Delayed; D007371:Interferon-gamma / Q000096:biosynthesis; D007376:Interleukin-2 / Q000378:metabolism; D008214:Lymphocytes / Q000378:metabolism*; D008875:Middle Aged; D015375:Receptors, Interleukin-2 / Q000096:biosynthesis*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D015704:CD4 Antigens; D016827:CD8 Antigens; D007376:Interleukin-2; D015375:Receptors, Interleukin-2; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D001151:Arsenic