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)

Kidneys from patients with lupus nephropathy, non-lupus immune-complex glomerulonephritis and other renal diseases were examined by indirect immunofluorescence for antigens related to a C-type virus from human cells (HEL-12 virus). All 11 specimens of lupus nephropathy contained HEL-12 virus antigens deposited in the same pattern as the immune complexes. The intensity of immunofluorescence with anti-HEL-12 virus serum correlated with the extent of immune-complex deposition. In contrast, nine renal lesions other than lupus nephropathy and seven normal tissues did not react with anti-HEL-12 virus serum. Antibody eluted from one kidney with lupus nephropathy reacted by indirect immunofluorescence with human and dog cells infected with HEL-12 virus but not with uninfected control cells. These findings demonstrate a specific association of lupus nephropathy with a C-type viral antigen that is deposited as antigen-antiviral antibody complex.
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PMID:C-type virus expression in systemic lupus erythematosus. 18 76

An antigen recognized by antisera produced against p30 (core) proteins of the four chief groups of mammalian type C viruses (murine, feline, RD-114 related to endogenous primate, and infectious primate group) is located in an immune-complex pattern in some renal glomeruli of human SLE patients with lupus proliferative glomerulonephritis but is not detected in normal or pathological control human kidneys. This antigen cross-reacts with p30 interspecies determinants shared by the four chief virus groups and cross-reacts with a partially purified antigen extracted from human SLE spleen. The human SLE spleen antigen cross-reacts with p30 group antigen of RD-114 virus but not of feline or murine viruses. Some host immunoglobulins eluted from a human SLE kidney by acid-buffer show antibody-like activity against p30 group antigen of RD-114 virus but not of simian, feline, or murine viruses.
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PMID:Type C RNA virus expression in systemic lupus erythematosus. New Zealand mouse model and human disease. 20 82

Postmortem study of proliferative glomerulonephritis associated with human systemic lumpus has previously shown that an antigen related to mammalian type C RNA viral core (p30) proteins is deposited in the renal glomerular lesions with human immunoglobulins in an immune-complex pattern. In the present work, human immunoglobulins were sequentially eluted from the lupus glomerular immune deposits and were assayed by a sensitive enzymoimmunoassay developed for the measurement of anti-p30 antibody activity against purified viral p30 proteins of mammalian type C viruses. Human immunoglobulins showing specific anti-p30 antibody activity, particularly against p30 antigen of feline endogenous virus RD-114 and to a smaller extent against p30 antigen of murine type C virus, were eluted by acid buffer from the glomerular immune deposits in two patients with lupus proliferative glomerulonephritis who have deposits of viral p30-related antigen in the same tissue lesions. This study adds support for the hypothesis that expression of type C viral antigen may be involved in the multifactorial pathogenesis of proliferative glomerulonephritis associated with human systemic lupus.
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PMID:Type C RNA virus-specific antibody in human systemic lupus erythematosus demonstrated by enzymoimmunoassay. 20 65

Endogenous retroviral gp70 was investigated as a participant in the pathogenesis of a lupus-like disease that spontaneously develops in four kinds of mice (NZB, NZB x W MRL/1, and male BXSB). Sera from these strains contain a heavy form of gp 70 that varies in sedimentation rates from 9S to 19S in sucrose density gradient analysis and appears with the onset of disease and persists throughout its course. Immunologically normal strains of mice do not develop rapidly sedimenting gp70 by 8-10 mo of life. The fact that the heavy gp70 is selectively absorbed with anti-IgG antibodies or with Staphylococcus aureus protein A suggests that it is complexed with antibodies. The incidence and quantities of these gp70 ICs rise with the progression of disease in all strains with lupus. These findings suggest that Ig-complexed heavy gp70 may be involved in the pathogenesis of glomerulonephritis of mice with SLE.
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PMID:Association of circulating retroviral gp70-anti-gp70 immune complexes with murine systemic lupus erythematosus. 22 10

G(IX) congeneic mouse strains, C57BL/6-G(IX) (+)(B6-G(IX) (+)) and 129-G(IX) (-), have been derived from the prototype strains, B6(G(IX) (-)) and 129(G(IX) (+)). The hybrids, (B6-G(IX) (+) x 129)F(1) (G(IX) (+)F(1)) and (B6 x 129-G(IX) (-))F(1) (G(IX) (-)F(1)), differ only in regard to genetic loci controlling G(IX) antigen expression. G(IX) (+)F(1) mice spontaneously produce G(IX) antibody and often show signs of autoimmune disease and lymphoproliferative disease. G(IX) (-)F(1) mice and mice of the two parental strains (B6-G(IX) (+) and 129) of G(IX) (+)F(1) do not produce G(IX) antibody and seldom show signs of these diseases. G((ERLD)), and G((RADA1)), antibodies, natural thymocytotoxic autoantibody, and antinuclear antibodies were produced by G(IX) (+)F(1) mice. However, these four antibodies were also found in the other strains. G(IX) (+)F(1) mice develop pronounced diffuse glomerulonephritis similar to that found in systemic lupus erythematosus in man. Incidence studies in which mice were examined according to age rather than state of health showed that the lesions occurred in 38% of G(IX) (+)F(1) mice but not in G(IX) (-)F(1), B6-G(IX) (+), or 129 mice. Lymphoproliferative lesions were either reticulum cell sarcoma (RCS) type A or reactive lymphoid hyperplasia (RLH). RCS occurred more often in G(IX) (+)F(1) (38%) than in G(IX) (-)F(1) (12%) or B6-G(IX) (+) (8%). No RCS occurred in mice of the 129 strain. RLH occurred in G(IX) (+)F(1) mice (10%) but not in the other strains. From these results, the following conclusions are drawn: (i) Severe glomerulonephritis and the increased occurrence of lymphoproliferative lesions in these animals depend on the presence of G(IX) antigen; (ii) besides genes controlling G(IX) antigen expression, other genes from both parental strains are required to create the basis in the progeny F(1) mice for the development of these diseases; and (iii) the chronic production of G(IX) antibody may be necessary for the development of the severe glomerulonephritis and for the increased occurrence of lymphoproliferative diseases in G(IX) (+)F(1) mice.
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PMID:Autoimmune and lymphoproliferative disease in (B6-GIX+ X 129)F1 mice: relation to naturally occurring antibodies against murine leukemia virus-related cell surface antigens. 22 83

The pathology of 1058 samples of kidney tissue studied during the past seven years as part of the renal biopsy service in Auckland is reviewed. About half of the samples were examples of glomerulonephritis, with diffuse proliferative and exudative glomerulonephritis being the most common finding. In the group of focal glomerular disease, lupus nephropathy and Goodpasture's Syndrome were frequently diagnosed.
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PMID:Renal biopsy pathology in Auckland, 1969-1976. 27 72

Adult female (NZB/NZW)F1 hybrid mice with documented autoimmune glomerulonephritis resembling systemic lupus erythematosus were treated with fractionated total lymphoid irradiation (TLI), a modification of the radiotherapeutic regimen currently used for the treatment of Hodgkin disease. After TLI, proteinuria subsided in all mice that had undergone radiotherapy, and the mean survival increased from 359 days in untreated controls to 545 days. It is suggested that TLI should be further investigated as a new approach for immunoregulation of autoimmune disorders.
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PMID:Successful treatment of autoimmune disease in (NZB/NZW)F1 female mice by using fractionated total lymphoid irradiation. 29 44

Significant differences in both specificity and avidity of anti-DNA antibodies were observed in the sera of groups of patients with active systemic lupus erythematosus glomerulonephritis, active systemic lupus erythematosus without nephritis, and in IgG eluates obtained by DNAase digestion of isolated glomeruli from glomerulonephritic kidneys. With methylated albumin-kieselguhr fractionated 3H-HeLa DNA as a source of native or single-strand DNA antigen in a modified Farr assay, an increased level of antibody to native DNA was associated with active systemic lupus erythematosus, particularly active nephritis. The avidity of antinative DNA estimated from plots of the reciprocals of bound and free antigen according to the Sips distribution formula was significanly lower in active glomerulonephritis sera than in sera from patients with active systemic lupus erythematosus without nephritis. However, antinative DNA of uniformly high avidity was found in the glomerular eluates. Avidity of single-strand DNA antibodies did not differ in the various patient groups. The data stronly supprot a major role for high avidity antinative-DNA in DNA/antiDNA immune complex-induced glomerular injury in systemic lupus erythematosus.
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PMID:Avidity of anti-DNA antibodies in serum and IgG glomerular eluates from patients with systemic lupus erythematosus. Association of high avidity antinative DNA antibody with glomerulonephritis. 29 48

Anti-native DNA antibodies have been evaluated in forty-six lupus patients' sera for antigen-binding capacity, affinity and precipitating activity. Diffuse proliferative glomerulonephritis was significantly correlated with the presence of high serum level of free anti-native DNA antibodies. Weak affinities were more often found in patients with than without glomerular changes but several patients had high-affinity anti-DNA antibodies and severe glomerulonephritis. No correlation was found between anti-DNA antibody-precipitating activity and renal lesions.
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PMID:Relationships between antibodies to native DNA and glomerulonephritis in systemic lupus erythematosus. 30 65

The investigation of the fine specificities of antinuclear antibodies (ANAs) has been fruitful in terms of the nosology and immunopathogenesis of human autoimmune syndromes. Particular reactivities serve as "markers," in that patients with certain syndromes have a much higher incidence of such ANAs than do patients with other diseases. In this category is the almost exclusive against the nuclear acidic protein Sm. Reactivity to Sm can be detected by precipitation in agar, complement fixation, or passive hemagglutination (1,2). Autoimmune mouse strains have also provided a fertile field for the investigation of the basic phenomena of self-activity. In particular, the NZB strain and its hybrid NZB x NZW have been considered excellent models for human SLE and have therefore been studied in great detail (3,4). In addition, Murphy et al at The Jackson Laboratory, Bar Harbor, Maine, have developed several new inbred mouse strains that spontaneously develop SLE-like syndromes (5,6). These are the BXSB strain, which has a male dominant disease characterized by little antiative DNA antibody; the MRL/1, which develops massive, nonmalignant lymphadenopathy, associated with enormous increases in serum immunoglobulin levels and fulminant renal disease; and the MRL/n, which does not develop SLE-like disease until well into the 2nd yr of life, but like the MRL/1 develops high titers of ANA and fatal glomerulonephritis. The MRL/1 differs from MRL/n in only about 10 percent of its genome, including the gene responsible for the MRL/1's lymphoproliferation. In the current study, we have used the technique of double immunodiffusion (ID) in agarose with standard human reference sera (of known ANA specificity) to survey a large number of mice from the NZB x NZW, MRL/1, MRL/n, BXSB, and other strains. We report here the finding of the anti-Sm marker" antibody almost uniquely in MRL/1 and MRL/n animals. These two related strains may serve as experimental models to explore the mechanism stimulating the production of this unique autoantibody in SLE.
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PMID:Presence of anti-Sm reactivity in autoimmune mouse strains. 30 83


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