Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in vitro response of lymphocytes to dsDNA, Sm, and Pokeweed Mitogen (PWM) and the role of monocytes in the control of this response were studied in 21 SLE and 14 healthy individuals. Specific hemolytic plaque assays were used to enumerate peripheral blood B lymphocytes secreting anti-dsDNA and anti-Sm antibodies. After 7 days in tissue culture without stimulation, anti-dsDNA or anti-Sm Plaque Forming Cells (PFC) were observed in 75% of SLE patients and 45% of normals. PWM, dsDNA, and Sm stimulation raised the levels of anti-dsDNA PFC in 25%, 37%, and 83% of SLE cultures respectively, and in all but one normal culture. PWM and dsDNA induced a decrease in anti-dsDNA PFC in 50% and 62% of SLE cultures. This suppressive effect was mainly exerted on spontaneous high producers of anti-dsDNA PFC. Monocyte depletion from cultures resulted in a decrease in PFC formation in all normals studied and in 7 SLE cultures. In 2 SLE cultures with no stimulation and one dsDNA stimulated culture, the number of anti-nuclear PFC increased after monocyte depletion. In cocultures of allogeneic, HLA-DR identical mononuclear cells, dsDNA pulsed SLE monocytes appeared more efficient than pulsed normal monocytes in helping to generate anti-dsDNA PFC. SLE lymphocytes responded less well than normals to dsDNA. These results suggest that: nuclear antigens may act as stimulators or suppressor of the specific autoimmune response, depending on the immune status of the SLE patient; and that abnormalities in both monocyte and lymphocyte responses lead to the excessive secretion of anti-dsDNA and anti-Sm antibodies by SLE B lymphocytes.
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PMID:Cellular control of antinuclear antibody production. Anti-dsDNA and anti-Sm plaque forming cells in SLE patients and normal individuals. 388 4

Normal human peripheral blood lymphocytes cultured in vitro with lupus sera (LS) were studied for their possible immunoglobulin (Ig) secretion using reverse haemolytic plaque assay (RHPA). Plaque forming cells (PFC) produced in cultures with LS (2,323 +/- 858 PFC/10(6) cultured cells) significantly increased in number compared to the control cultures with normal human serum (206 +/- 43, P less than 0.05). However, the artifactual nature of the PFC formation due to cytophilic Ig in LS subsequently became evident from the kinetic curves, trypsinization or medium change at the end of the culture period, radiation of cells on the first day of culture, or by depletion of nylon wool column-adherent cells from the culture system. These cytophilic Ig were observed in 56% of the sera obtained from untreated lupus patients. Thus, their possible interference with the resultant spurious plaque formation might be difficult to eliminate when performing RHPA in lupus patients.
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PMID:Pseudoplaque formation by cytophilic immunoglobulins in the sera of lupus patients as measured using reverse haemolytic plaque assay. 704 57

Idiotype (Id) 16/6 marks a variable (V) region structure that occurs frequently in the human immunoglobulin repertoire. The basis of the Id has been traced to a germline heavy chain gene segment, VH18/2 (VH26). To pursue the molecular basis for the frequency of Id 16/6, we have analyzed polymerase chain reaction-generated C mu, C gamma, and VH3 family V gene libraries derived from the circulating and tonsillar B cells of four normal individuals and from the B cells of two patients with active systemic lupus erythematosus (SLE). The frequency of VH18/2 in these libraries was compared with three control VH genes, VH56P1, VH21/28, and VHA57. Plaque lifts from C mu and C gamma VH cDNA libraries were screened with gene-specific oligonucleotide probes. The frequency of VH18/2 ranged from 4 to 10% of JH+ plaques (two of five times that of control VH genes). In four VH3 family-specific libraries derived from rearranged DNA, VH18/2 represented 19-33% of VH3+ plaques. Hybridizing VH18/2 plaques were 98-100% homologous to the germline VH gene; mutations when present were often in framework 3. Extensive variation was seen in the complementarity determining region 3 sequences of these rearranged V genes. The high frequency of VH18/2 expression in the B cell repertoire was confirmed by sequencing randomly picked JH+ plaques. In two patients with active SLE the frequency of use of VH18/2 was not greater than that observed in normal subjects. These results show that VH18/2 is overrepresented in the B cell repertoire of normal subjects and suggest that the immune repertoire may be dominated by relatively few V genes.
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PMID:High-frequency representation of a single VH gene in the expressed human B cell repertoire. 845 18

Accumulating data suggest that endocrine disruptors affect not only the reproductive system, but also the immune system. We demonstrate here that endocrine disruptors including diethylstilbestrol (DES) and bisphenol-A (BPA) enhance autoantibody production by B1 cells both in vitro and in vivo. BWF1 mice, a murine model for systemic lupus erythematosus (SLE), implanted with Silastic tubes containing DES after orchidectomy developed murine lupus characterized by immunoglobulin G (IgG) anti-DNA antibody production and IgG deposition in the glomeruli in the kidney as well as those implanted with 17beta-estradiol (E2). Plaque-forming cells (PFC) producing autoantibodies specific for bromelain-treated red blood cells were significantly increased in mice implanted with DES and BPA. IgM antibody production by B1 cells in vitro was also enhanced in the presence of endocrine disruptors including DES and BPA. Estrogen receptor (ER) expression was upregulated in B1 cells in aged BWF1 mice that developed lupus nephritis. These results suggest that endocrine disruptors are involved in autoantibody production by B1 cells and may be an etiologic factor in the development of autoimmune diseases.
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PMID:Endocrine disruptors (environmental estrogens) enhance autoantibody production by B1 cells. 1516 99

Morphea is an uncommon connective tissue disease with the most prominent feature being thickening or fibrosis of the dermal without internal organ involvement. It is also known as a part of localized scleroderma. Based on clinical presentation and depth of tissue involvement, morphea is classified into several forms, and about two thirds of adults with morphea have plaque type. Overproduction of collagen production by fibroblast is the cause of abnormality in morphea, and the hyperactivity mechanism of fibroblast is still unknown, although there are several mechanisms already proposed. Plaque type morphea is actually a benign and self limited. Plaque type morphea that mimicking systemic lupus erythematosus in clinical appearance, such as alopecia and oral mucosal ulcers, is uncommon. A case of plaque type morphea mimicking systemic lupus erythematosus in a 20 year old woman was discussed. The patient was treated with local and systemic immunosuppressant and antioxydant. The patient's condition is improved without any significant side effects.
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PMID:A patient with plaque type morphea mimicking systemic lupus erythematosus. 2626 May 57