摘要
Background:Localized scleroderma (LSc) exhibits autoimmunity, and antihistone antibody is frequently detected. The major antigens recognized by antihistone a ntibody are histones H1, H2AandH2B,whicharelocatedontheoutersideofthenucleosome and are relatively more accessible for antibody binding. Therefore, it has been hypothesized that antihistone antibody is induced by nucleosome or native chroma tin as immunogens in LSc. Objectives:To determine whether antinucleosome antibo dy is present in patients with LSc. Methods:Antinucleosome antibody, antihiston e antibody and antidouble-stranded DNA (dsDNA) antibody were determined by enzy me-linked immunosorbent assay. Results:IgG or IgM antinucleosome antibody was detected more frequently in patients with LSc than was antihistone antibody:in 40 of 49 (82%) vs. 26 of 49 (53%), respectively. No patients had anti-dsDNA a ntibody. The prevalence of antinucleosome antibody positivity was comparable in the three subgroups of LSc (generalized morphoea, 89%; linear scleroderma, 71% ; morphoea, 90%). Patients with systemic lupus erythematosus (SLE) exhibited a similar frequency of antinucleosome antibody positivity (13 of 15, 87%), but th eir IgG levels of this autoantibody were much higher than those found in patient s with LSc. By contrast, IgM antinucleosome antibody levels were normal in patie nts with SLE, while they were significantly increased in patients with LSc compa red with normal controls. Antinucleosome antibody was also detected at lower fre quency in patients with systemic sclerosis(fiveof20,25%)ordermatomyositis(fiveo f15,33%). Nucleosome-restricted antibodies, i.e. antibodies that react with th e whole nucleosome particle but not with its individual components (histones and dsDNA) were also present in 35%of patients with LSc. Conclusions:Although ant inucleosome antibody was not specific to LSc, its high prevalence in LSc indicat es that antinucleosome antibody is a major autoantibody in this disease.
Background:Localized scleroderma (LSc) exhibits autoimmunity, and antihistone antibody is frequently detected. The major antigens recognized by antihistone a ntibody are histones H1, H2AandH2B,whicharelocatedontheoutersideofthenucleosome and are relatively more accessible for antibody binding. Therefore, it has been hypothesized that antihistone antibody is induced by nucleosome or native chroma tin as immunogens in LSc. Objectives:To determine whether antinucleosome antibo dy is present in patients with LSc. Methods:Antinucleosome antibody, antihiston e antibody and antidouble-stranded DNA (dsDNA) antibody were determined by enzy me-linked immunosorbent assay. Results:IgG or IgM antinucleosome antibody was detected more frequently in patients with LSc than was antihistone antibody:in 40 of 49 (82%) vs. 26 of 49 (53%), respectively. No patients had anti-dsDNA a ntibody. The prevalence of antinucleosome antibody positivity was comparable in the three subgroups of LSc (generalized morphoea, 89%; linear scleroderma, 71% ; morphoea, 90%). Patients with systemic lupus erythematosus (SLE) exhibited a similar frequency of antinucleosome antibody positivity (13 of 15, 87%), but th eir IgG levels of this autoantibody were much higher than those found in patient s with LSc. By contrast, IgM antinucleosome antibody levels were normal in patie nts with SLE, while they were significantly increased in patients with LSc compa red with normal controls. Antinucleosome antibody was also detected at lower fre quency in patients with systemic sclerosis(fiveof20,25%)ordermatomyositis(fiveo f15,33%). Nucleosome-restricted antibodies, i.e. antibodies that react with th e whole nucleosome particle but not with its individual components (histones and dsDNA) were also present in 35%of patients with LSc. Conclusions:Although ant inucleosome antibody was not specific to LSc, its high prevalence in LSc indicat es that antinucleosome antibody is a major autoantibody in this disease.
