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)

To test the potential role of autoimmunity to the highly conserved heat shock proteins (HSP) in immune arthritides, the sera from 99 patients with rheumatoid arthritis (RA), 48 patients with systemic lupus erythematosus (SLE) and 65 normal controls were examined by ELISA for IgG and IgM antibodies to the 65 kDa and 70 kDa heat shock proteins from Mycobacterium bovis (Bacille Calmette-Guerin; BCG). In RA sera there are significant numbers of individuals with increased IgM anti-65 kDa and anti-BCG reactivity as well as IgG anti-70 kDa when compared with controls. In SLE both IgM and IgG anti-BCG, together with IgM anti-65 kDa, differed significantly from controls. The results were compared with previous reports in similar groups of patients, and it is clear that no consistent pattern of reactivity emerges. While further work may be justified looking carefully at the disease duration and other subsets of both RA and SLE, it is difficult at this stage to conclude that antibodies to autologous HSP that cross-react with mycobacterial HSP play a major role in disease pathogenesis.
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PMID:Antibodies to 65 kDa and 70 kDa heat shock proteins in rheumatoid arthritis and systemic lupus erythematosus. 147 94

The authors report a case of lupus vulgaris in a 22-year-old female patient occurring three months after BCG vaccination, with a period of evolution of two months. The Mantoux intradermoreaction (1 U) was strongly positive, and no acid-fast bacilli were found in the lesion, either by direct analysis or by culture in a Lowenstein medium. The histopathological findings confirmed the diagnosis. Prescribed treatment with isoniazid and rifampicin for three months resulted in complete healing on the sixth month.
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PMID:[Lupus vulgaris after BCG vaccination. A clinical case]. 207 7

The in vivo effects of a variety of inflammatory stimuli on complement C4 and factor B plasma levels have been examined. MRL/++ (H-2k) mice were given intraperitoneal injections of lipopolysaccharide, turpentine, Corynebacterium parvum pyridine extract residue or high doses of indomethacin. All of these treatments induced an increase in plasma factor B concentrations, which in the case of C. parvum was dose dependent and persisted for at least 7 days. Lipopolysaccharide, turpentine and indomethacin produced decreases in plasma complement C4. C. parvum, however, produced an increase in plasma complement C4 to approximately 240% of controls which was independent of gender. It was also independent of major histocompatibility complex haplotype, since the same effect was seen in C57B1/6J-bg/bg and C57B1/6J-bg/+ mice. The gross increment in complement C4 was, however, related to the major histocompatibility complex. H-2K mice ("low complement C4") had smaller increments than H-2b ("high complement C4"). Mycobacterium bovis (BCG) also produced a transient increase in C4 in the H-2b mice as well as a prolonged increase in factor B levels. These data (i) suggest that different inflammatory stimuli induce different mediators which may have differential effects on factor B and complement C4 synthesis, and (ii) emphasize the independent regulation of complement C4 and factor B. Qualitative variations in the mediators elaborated during chronic inflammatory diseases may help determine complement C4 fluctuations in systemic lupus erythematosus and the wide range of complement C4 concentrations seen in MRL/1 pr mice with active immune complex disease.
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PMID:Differential effect of inflammatory stimuli on murine plasma C4 and factor B concentrations. 305 73

Classical models of experimental autoimmune diseases, such as adjuvant arthritis entail the use of mycobacteria. Furthermore, BCG immunotherapy may be followed by arthritic symptoms. To test the infection-autoimmunity relationship of mycobacteria, we used monoclonal antibodies raised against M. tuberculosis and against DNA. Murine monoclonal anti-TB antibodies were found to react with ssDNA, dsDNA and other polynucleotides. Monoclonal anti-DNA autoantibodies derived from patients and mice with SLE bound to three glycolipids shared among all mycobacteria and derived from mycobacterial cell wall. Prior incubation of the antibodies with ssDNA and other polynucleotides or with glycolipid antigens inhibited binding. These results indicate that infecting mycobacteria share antigens with human tissue, thus accounting in part for the production of autoantibodies in mycobacterial infections.
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PMID:Monoclonal anti-tuberculosis antibodies react with DNA, and monoclonal anti-DNA autoantibodies react with Mycobacterium tuberculosis. 310 32

In the developed industrial countries, the frequency of tuberculotic diseases of the skin including lupus has decreased to a very low level because of the significant decline of morbidity and mortality, the elimination of Bovine infections, the introduction of BCG vaccination, as well as effective anti-tuberculotic drugs employed for about 30 years. In spite of the very favorable therapeutic results, we have to reckon with the continuance of the present lupus incidence as long as the number of tuberculotic affections in the world is about 20 million, and even in developed industrial countries, the yearly rate of tuberculotic patients amounts to 43 in 100,000 inhabitants. We know that the disease still occurs very frequently in the developing countries of the Far East.
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PMID:[Lupus vulgaris (tuberculosis cutis luposa). Clinical aspects and therapy past and present]. 390 61

NZB/NZW F1 hybrid mice develop a spontaneous autoimmune disease characterized by the appearance of antinuclear antibodies and premature death due to immune complex glomerulonephritis. To investigate the possible effects of cellular immune stimulation on this disorder, groups of female NZB/NZW mice, aged 2, 5, and 7 months, were treated either with the nonspecific immunostimulatory agent Mycobacterium bovis strain BCG or with saline. Mice treated with BCG at ages 5 and 7 months died sooner than age-matched controls, and death was associated with severe glomerulonephritis, suggesting that BCG may have accelerated autoimmunity in these mice. Since BCG is known to stimulate the production of type II (or gamma) interferon, a substance with potent immunoregulatory effects, a second study was carried out to assess the effects of type II interferon on NZB/NZW disease. A greater number of type II interferon-treated mice died by 9 months of age when compared to controls, and the increased death rate was associated with a more rapid development of antinuclear antibodies and histologically confirmed glomerulonephritis. These data, together with a recent report of increases in the level of serum type II interferon in patients with active systemic lupus erythematosus, suggest that type II interferon may play a role in the pathogenesis of autoimmune disease.
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PMID:Treatment of NZB/NZW F1 hybrid mice with Mycobacterium bovis strain BCG or type II interferon preparations accelerates autoimmune disease. 617 32

The authors report on an exceptional complication of BCG vaccination: a case of facial lupus vulgaris, which appeared one year after vaccination in a girl with normal cellular and humoral immunity.
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PMID:[Facial lupus vulgaris caused by BCG]. 665 53

A case of intradermal BCG vaccination was complicated by a lupus-like tuberculosis cutis progressive for over 30 years. The patient had been vaccinated twice with BCG in the affected site. A review of other BCG vaccine-induced cases of lupus vulgaris indicates that the incidence of this complication is markedly increased following multiple BCG vaccinations, but is rare following a single BCG vaccination. In our patient a skin biopsy specimen was characteristic for lupus vulgaris. Acid-fast stains from the tissue and cultures from the affected site were negative. The patient was successfully treated with rifampin.
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PMID:BCG vaccine-induced lupus vulgaris. 706 66

NOD mice spontaneously develop organ-specific autoimmunity and are widely used as a model for diabetes. NOD mice also exhibit some features of non-organ specific autoimmune rheumatic disease such as thymocytotoxic and anti-nuclear autoantibodies and they develop haemolytic anaemia in senescence. A single dose of 2.6 x 10(7) heat-killed Bacillus Calmette-Guerin (BCG) i.v. in 8-week-old NOD mice prevented diabetes but precipitated a syndrome similar to systemic lupus erythematosus (SLE), in which treated mice rapidly developed haemolytic anaemia, high titre anti-DNA and anti-Sm antinuclear autoantibodies, perivascular lymphocytic infiltration in the kidneys and glomerular immune complex deposition. Here, we examined the mechanism of action by which BCG precipitated rheumatic autoimmune disease in NOD mice. Two weeks after injection, reticuloendothelial cell function was dramatically increased in BCG-treated NOD mice. By 4 weeks, treated mice had a three- to four-fold increase in Mac-1+ and class-II+, B220-negative splenocytes and in vitro antigen-presentation capacity was enhanced two- to four-fold. In vivo responses to SRBC confirmed enhancement of DTH 4 weeks after BCG injection, consistent with an adjuvant-like activity.
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PMID:Mycobacteria precipitate autoimmune rheumatic disease in NOD mice via an adjuvant-like activity. 800 75

The authors report a case of association between lupus vulgaris and urticarial vasculitis after BCG vaccination. Lupus vulgaris is a rare classical complication of BCG vaccination. Anaphylactoid reactions after BCG are very rare. This is the first report of association between the two diseases after BCG and the third report of urticaria after BCG. The pathogenesis of this is discussed.
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PMID:[Systemic urticaria disclosing post-vaccine lupus tuberculosis]. 823 64


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