lewis-x-antigen and Lupus-Erythematosus--Systemic

Immune complexes are present in the circulation of healthy individuals and the formation of such complexes is part of a normal immune process. During some pathological conditions, significant amounts of immune complexes are formed and deposited in the kidney and other tissues, causing severe injury. Since the levels of immune complexes can provide valuable prognostic information, dozens of methods have been developed to detect and quantify these complexes. However, many of these methods are non-specific, not quantitative, and give false-positive results. Methods based on detecting the antigen portion of immune complexes can yield more precise information about circulating immune complexes. We have used a quantitative dot-blot assay, which permits detection of antigen even if buried, to determine the levels of antigen in circulating immune complexes. In healthy donors, significant amounts of immune complexes containing DNA and beta(2)-glycoprotein I were detected (natural immune complexes). Natural immune complexes with Lewis X antigen were also observed in the circulation of healthy persons. In experimentally induced murine systemic lupus erythematosus (SLE) and SLE patients, there was a correlation between the clinical manifestations and the levels of DNA in the circulating immune complexes. At severe SLE flares, the level of DNA in circulating immune complexes decreased, probably due to tissue deposition of immune complexes. The low levels of DNA in immune complexes circulating in SLE patients correlated with low serum concentrations of the complement component C1q. No direct correlation was found between the levels of circulating anti-dsDNA antibodies and DNA in immune complexes. Thus, quantitation of antigen levels in circulating immune complexes can be used to determine the prognosis of autoimmune diseases.

Topics: Adult; Animals; Antigen-Antibody Complex; Antigens; Autoantibodies; Autoimmune Diseases; beta 2-Glycoprotein I; DNA; Glycoproteins; Humans; Immunity, Innate; Immunoblotting; Lewis X Antigen; Lupus Erythematosus, Systemic; Mice; Prognosis

To study the in vitro modulation of autogeneic and allogenic regulatory T lymphocytes proliferation by bone marrow mesenchymal stem cells (MSCs) in patients with systemic lupus erythematosis (SLE).. Human MSCs were separated with Percoll (1.073 g/ml) from bone marrow of patients with SLE or healthy subjects. The purity of MSCs was identified with the phenotypes by fluorescence active cell sorter (FACS). The subset regulatory T cells in the peripheral blood of patients with SLE were isolated with magnetic activated cell sorting (MACS) CD4 and CD25 microbeads. Lymphocytes or CD4+ CD25+ T cells isolated from the peripheral blood of SLE patients were cocultured either with autologous MSCs or MSCs from healty donors. The proliferation activities of lymphocytes and CD4+ CD25+ T cells were investigated with methyl thiazolyl tetrazolium( MTr) test. The level of IL-10 and transforming growth factor beta (TGFbeta) was determined with enzyme-linked immunosorbent assay (ELISA).. The lymphocyte activity in SLE was suppressed by autogeneic and allogeneic MSCs and the inhibition rate was 56.32% and 65.46%, respectively. A stronger immunosuppressive effect of allogeneic MSCs was detected. MSCs were capable of increasing the proportion of allogeneic and autogeneic regulatory T cells in a dose dependent fashion. MSCs stimulated CD4+ CD25+ T cells to produce IL-10 and TGFbeta.. MSCs can suppress lymphocyte proliferation and increase CD4+ CD25+ T cells. MSCs might play important roles in immunosuppressant lymphocyte proliferation and be important to cooperate with autogeneic hematopoietic stem cells in transplantation.

Topics: Adolescent; Adult; Cell Proliferation; Cells, Cultured; Enzyme-Linked Immunosorbent Assay; Female; Humans; Interleukin-10; Lewis X Antigen; Lupus Erythematosus, Systemic; Male; Mesenchymal Stem Cell Transplantation; Mesenchymal Stem Cells; Middle Aged; T-Lymphocytes, Regulatory; Transforming Growth Factor beta

The antigen/receptor specificity of antigranulocyte antibodies (AGAs) detected in the sera of patients with systemic lupus erythematosus (SLE) was investigated by inhibitory immunofluorescence test and Western immunoblotting technique. The interactions of AGAs with antigens of intact normal granulocytes were determined by inhibiting the binding of different myeloid monoclonal antibodies (mAbs). Seven of the studied 12 sera revealed binding to CD15 (X hapten) and/or to CD16 (FcR1o). The specificity investigation of AGAs was completed with Western immunoblotting technique. The binding of AGAs to bands with Mr of about 50-60 kDa and at 30 kDa on unstimulated granulocyte plasma membrane preparation could be demonstrated from 4 out of 6 AGA positive SLE sera. The cause of the disappearance of bands on the phorbol-myristate-acetate (PMA) activated membrane except those of the 50-60 kDa bands is still to be discovered.

Topics: Adult; Antibody Specificity; Antigens, Differentiation; Autoantibodies; Autoantigens; Blotting, Western; Female; Glycolipids; Granulocytes; Humans; Lewis X Antigen; Lupus Erythematosus, Systemic; Male; Receptors, Fc; Receptors, IgG; Receptors, Immunologic