Objective:To study the relationship between the dose of active DNA and the induction of SLE-like syndrome.Methods: DNA from extracted ConA-activated spleen lymphocytes and immunized syngenic mice with different quantities of active DNA, the anti-dsDNA antibodies and anti-histone antibodies as well as the antibody subclass were detected by ELISA.The patterns of antinuclear antibodies and immune complexes in glomeruli were observed by immunofluorescent-stain. Results: 10 pig active DNA could induce all the animal to produce anti-dsDNA and anti-histone antibodies,and the induced autoann'bodies were mainly IgGl type.Only 25%animals produced autoantibodies immunized by 5 fjig active DNA. Conclusion:The minimum dose of active DNA to induce SLE-like syndrome was 10 ^tg,and it predominantly evoked the humoral response.

Objective To study the immunogenicity of extractable nuclear antigens(ENA)in activateed lymphocytes.Methods The ENA of the normal and activated lymphocytes was extracted according to Sharp's method,then syngeneic BALB/C mice were immunized.The dynamic fluctuation of serum IgG anti-dsDNA antibody level in mice was analyzed by ELISA,so did the ENA polypeptide spectrum.The immunofluorescent staining pattern of ANA and renal immunopathologic changes of the mice were investigated.Results ANA could be detected in the sera of the immunized mice by the ENA extracted from the activated lymphocytes,including anti-dsDNA and anti-ENA.The immunofluorescent staining patterns for ANA manifested as homogeneous pattern,peripheral pattern,speckled pattern and nucleolar pattern.Moreover,marked immune complex deposits in glomerulus could be observed in ANA positive mice.The results in those mice immunized by the normal-lymphocyte-ENA were negative.Conclusion The ENA extracted from activated lymphocytes is immunogenic,can drive the production of ANA and cause SLE-like syndrome.

Objective To study the effect of human prolactin (PRL) on total IgG and anti-dsDNA antibody production in peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE). Methods PBMC from SLE patients and control subjects were cultured, with the stimulation of PRL, interleukin 2 (IL-2), interleukin 10 (IL-10) and phytohemagglutinin (PHA). 3H-thymidine (3H-TdR) incorporation assay was used to study the proliferation of PBMC. Total IgG and anti-dsDNA antibodies in the cultured supernatants were measured by enzyme-linked immunosorbent assay (ELISA) in 19 patients of SLE and in 6 control subjects. Results ①The proliferation of PBMC in vitro was enhanced by 10-9 mol/L PRL in 19 patients of SLE. ②The production of IgG and anti-dsDNA antibodies in PBMC from 10 active SLE patients was much higher than that of 9 inactive patients (P

Objective To investigate the primary autoantigens which contribute to the production of anti-DNA antibodies. These antibodies are serological hallmark and pathogenic factor of systemic lupus erythematosus (SLE).Methods Nonautoimmune predisposed BALB/c mice were immunized with concanavalin A (Con A) activated, lipopolysaccharide (LPS) activated and nonactivated syngeneic spleen cells. Nuclei and chromatin from activated/nonactivated lymphocytes were isolated and syngeneic mice were immunized. Sera were taken after the third immunization. IgG anti-dsDNA antibody was determined by ELISA (calf thymus DNA treated with S1 nuclease was used as the coated antigen). The glomerular IgG deposition was observed by immunofluorescence one month after the third immunization.Results Con A activated T cells and LPS activated B cells induced anti-double stranded (ds) DNA antibody in syngeneic nonautoimmune BALB/c mice and formed the glomerular IgG deposition. Further studies showed that active chromatin isolated from activated lymphocytes induced anti-ds DNA antibody, but not resting chromatin isolated from nonactivated lymphocytes.Conclusions Activated lymphocytes and their active chromatin could be the autoimmunogen(s) driving the anti-dsDNA antibodies. The change of chromatin's antigenicity by environmental factors and genetic background may be the common pathway to SLE pathogenesis.