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)

A patient is described in which an inherited defect in the synthesis of C2 complement component coexisted with the disease systemic lupus erythematosus. The family studies show evidence of the autosomal recessive nature of the inheritance of the C2 synthesis defect. Of particular interest was the finding of a great-aunt who also had homozygous C2 deficiency. This great-aunt suffered from discoid lupus erythematosus as well. The occurrence of various autoantibodies in the serum from the family members, the typing for blood groups, HL-A antigens, and some serum protein markers are reported and discussed. The C2 deficiency may be a critical defect in the host defenses to infection that predisposed to the development of autoimmune disease.
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PMID:Inherited C2 deficiency and systemic lupus erythematosus: studies on a family. 4 31

In 4 women lymphomas developed 2 months to 12 years after the onset of systemic lupus erythematosus. An association between the two diseases had previously been reported in 14 cases, in 6 of which the lymphoma either preceded or was diagnosed at the same time as the autoimmune disease. In systemic lupus erythematous early biopsy of suspect lymph-nodes is recommended.
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PMID:Systemic lupus erythematosus and lymphoma. 8 Jun 83

The age-dependent capacity of NZB and (NZB x NZW)F1 hybrid, BALB/c, DBA/2, C57BL/6 and C3H mice to generate T cell-mediated immune responses was assessed qualitatively and quantitatively by measuring the following effector functions: (a) the time course of alloreactive cytotoxic T-cell activity triggered in vitro was comparable for NZ and other mouse strains; cell reactivity generated in vivo against EL4 tumour cells was low in young (NZB x NZW)F1 mice and in DBA/2 mice but was comparable for older (NZB x NZW)F1, NZB and other mouse strains; (b) the time-dependent, vaccinia virus-specific, cytotoxic T-cell activity after systemic infection was similar for all mouse strains; (c) the T cell-dependent primary footpad swelling after local injection with lymphocytic choriomeningitis virus was within the same range for all mouse strains tested with respect to size and kinetics of the reaction; (d) the cell-mediated immune protection against Listeria monocytogenes after systemic infection revealed that NZ mice are, independent of age, more susceptible than C3H or C57BL/6 mice and comparable to A strain mice. Therefore, these responses in young, or clinically relatively normal older, NZB or (NZB x NZW)F1 strains that are affected by a lupus-like autoimmune disease did not differ markedly from the range of responses of other mouse strains of 2-14 months of age, which are not known to be similarly diseased. Thus, overall cell-mediated immunity of NZ mice as assessed quantitatively and kinetically in these functional models is within normal ranges. Possible T-cell defects may therefore be selective and either do not occur or were not detected in these models.
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PMID:Comparison of T cell-mediated immune responsiveness of NZB, (NZB x &NZW)F1 hybrid and other murine strains. 14 94

Reagents and equipment are now readily available to make fluorescent antibody techniques routine diagnostic procedures. Antinuclear antibodies are detectable by such methods and are useful in the diagnosis of autoimmune disease. By defining not only the site of tissue damage but also the specific components deposted at that site, immunofluorescence applied to renal biopsies has helped to elucidate the nature of otherwise similar appearing processes. Fluorescent techniques also facilitate diagnosis of such skin diseases as lupus, bullous pemphigoid and pemphigus.
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PMID:Diagnostic applications of the fluorescent antibody method. 17 15

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 immunological side-effects under treatment with antihypertensive drugs are mainly limited to autoimmunity and autoimmune disease caused by alpha-methyldopa and hydralazine. Autoimmune hemolytic anemia is more common during treatment with alpha-methyldopa. Hydralazine may induce antinuclear antibodies. Some patients develop a SLE-like syndrome. Its clinical picture is less severe and its prognosis is more favourable than that of spontaneous SLE. During treatment with low doses the disease develops exclusively in patients who are slow acetylators. It may appear also in rapid acetylators during the high dose treatment. The symptoms are usually reversible after withdrawal of the drug.
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PMID:Immunological side-effects of antihypertensive drugs. 28 3

Serial serum samples from NZB/NZW F1 mice were studied by sucrose density gradient ultracentrifugation and filter radioimmunoassay for the immunoglobulin class of antibodies to double-stranded DNA and single-stranded RNA (Poly A). These antibodies occur spontaneously during the course of an autoimmune disease resembling systemic lupus erythematosus. Study of serum samples at 2-week intervals showed the sequential appearance of 19S followed by 7S anti-nucleic acid antibodies, an earlier commitment to 7S antibodies in female compared to male mice, and an independent and unrelated switching mechanism (19S-7S) for antibodies to DNA and Poly A. The more severe disease in female mice is correlated with an earlier appearance of 7S anti-DNA antibodies. This sequential and ordered appearance of antibodies to nucleic acids is discussed in relation to possible immunologic regulatory mechanisms.
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PMID:Immunological regulation of spontaneous antibodies to DNA and RNA. II. Sequential switch from IgM to IgG in NZB/NZW F1 mice. 30 Mar 53

Administration of thymosin fraction V to NZB/NZW F1 mice, an animal model for human SLE, accelerated the appearance of proteinuria and anti-nDNA antibodies, increased deposition of immunoglobulins in kidneys, and significantly shortened survivals. Although the addition of thymosin to in vitro cultures of spleen and lymph node cells from thymosin-treated mice increased DNA synthesis in response to stimulation with Con A, in vivo treatment with thymosin did not affect the Con A response. There was no effect on in vitro responses to PHA or LPS, or on IgM antibody formation to SRBC (T cell dependent) or SSS III (T cell independent) immunizations. Antibodies to thymosin or contamination of our thymosin preparations with nucleic acids could not be demonstrated. The acceleration of autoimmune disease produced by thymosin treatment could not be explained by alteration of the T and B cell functions studied.
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PMID:Effect of altered lymphocyte function on immunologic disorders in NZB/NZW mice. III. Acceleration of disease by thymosin. 30 81

Four cases are described of multi-system immunologically-mediated disease (systemic lupus erythematosus (two cases), polymyositis, and sarcoidosis) in association with thyroid autoimmunity. In all patients there was evidence of T lymphocyte deficiency, namely poor response of peripheral blood lymphocytes (PBL) to T cell mitogens (four cases) and failure or decreased ability to become sensitized to dinitrochlorobenzene (three cases), although two patients were ill and two were being treated with steroids. There was also evidence of B lymphocyte deficiency since PBL of no patient responded normally to pokeweed mitogen, a B and T lymphocyte mitogen. In two patients there was evidence of cell-mediated immunity to human thyroid antigens. Although thyroid stimulating antibody was not detected in the one patient with Graves' disease tested, significant titres of thyroid antibodies were detected in all cases. Possible relationships between T lymphocyte deficiency, organ-specific autoimmune disease and immunologically-mediated multi-system disorders are discussed.
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PMID:Multi-system immunologically mediated disease: T lymphocyte deficiency and thyroid immunologic disease--a report of four cases. 30 99

This report describes a previously unrecognized animal model of SLE, the PN mouse. Although outbred PN mice were studied originally as models of polyarteritis nodosa, their inbred descendants have autoimmune disease which closely resembles SLE. In the current study, positive indirect immunofluorescence tests for ANA appeared when the mice were 5 months old, and 80% of mice were ANA-positive at 10 months of age. Anti-DNA were detected in sera from newborn mice and from 53% of mice under 2 months of age. Seventy-six percent of PN mice developed anti-DNA at the age of 10 months. Glomerular deposits of IgG, IgM, IgA, and complement appeared at 2 to 4 weeks of age, and examination of renal tissue by electron microscopy showed basement membrane thickening and dense intramembranous deposits. Neoplasms arose in 14% of PN mice. Female mice died earlier than male mice, and the most common causes of death were glomerulonephritis and arteritis. It was concluded that the serologic and histologic characteristics of disease in PN mice resembled SLE.
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PMID:Palmerston North mice, a new animal model of systemic lupus erythematosus. 31 Aug 56


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