Description of Systemic Lupus Erythematosus: A Historical Perspective

Graninger, W; Smolen, JS; Zielinski, C. C.

doi:10.1007/978-3-642-71642-3_1

“…The basic question of whether the autoimmune response results from an unusual presentation of certain antigens or from an abnormality or alteration of the immune system itself is still a matter of controversy. It has been suggested that several immunoregulatory mechanisms may be implicated and that certain agents such as viruses may play a role in eliciting autoantibodies (8)(9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Presence of antibodies to ubiquitin during the autoimmune response associated with systemic lupus erythematosus.

Muller

¹

,

Briand

²

,

Regenmortel

³

1988

Proc. Natl. Acad. Sci. U.S.A.

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Sera from patients with systemic lupus erythematosus (SLE) were shown to react with both ubiquitin and a synthetic fragment of it (residues 22-45) in an ELISA and with ubiquitin in immunoblotting experiments. Close to 80% of lupus patients possessed ubiquitin antibodies, whereas only 55% of them possessed native DNA antibodies, a marker of SLE. Less than 16% of patients with other rheumatic autoimmune diseases possessed antibodies to ubiquitin. Our results indicate that the combined measurement of antibodies to native DNA and to ubiquitin could appreciably increase the detection of SLE cases (up to 85% in our study). It is suggested that ubiquitin, a heat shock protein, could be involved in antibody formation against ubiquitin-protein conjugates present during cellular injury and that this represents a major characteristic of the autoimmune response in SLE.The immunopathology and etiology of systemic lupus erythematosus (SLE) have been intensely investigated in recent years. The most striking feature of rheumatic diseases, and of SLE in particular, is the large variety of induced clinical manifestations and the wide spectrum of autoantibodies found to react with different constituents of normal cells. The antigenic targets of autoantibodies found in SLE include a number of nuclear components (DNA,

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“…The Human SLE Syndrome Systemic lupus erythematosus (SLE) was first considered a multiphenotypic disease syndrome by Moritz Kaposi of Vienna in 1872 (1). At the beginning of this century SLE was already believed to be, at least in part, an immune disorder on the basis of observations of false-positive syphilis serology in some patients.…”

mentioning

confidence: 99%

“…Additionally, it was proposed that there are genetic as well as environmental components that contribute to this disease (1,5). Exposure to ultraviolet (UV) radiation, infection, diet, therapeutic drugs, physical and mental stress, and hormonal status (pregnancy) can have profound effects on the immune system and thus may contribute to the pathogenesis of SLE (3)(4)(5).…”

mentioning

confidence: 99%

New Zealand mixed mice: a genetic systemic lupus erythematosus model for assessing environmental effects.

Rudofsky

¹

,

Lawrence

²

1999

Environ Health Perspect

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Systemic lupus erythematosus (SLE) is a multiphenotypic autoimmune disease. The hallmark of SLE is the production of anti-double-stranded DNA autoantibodies and the deposition of immune complexes in target tissues such as the kidney, skin, and brain. Additional phenotypic traits are the presence of arthritis, anemia, central nervous system involvement, and a variety of autoantibodies. Females of childbearing age are particularly at risk. Recent genetic analysis of murine SLE shows that susceptibility is under complex polygenic control. It is also apparent that environmental factors contribute to the induction and exacerbation of SLE. We describe here the genotypic and phenotypic characterization of a group of recombinant inbred strains of SLE-prone mice that were derived from NZB and NZW progenitors, the parental strains of the classic female F1 hybrid lupus model. Recombination and reassortment of these ancestral genomes resulted in the NZM (New Zealand mixed) strains with strain-specific patterns of renal disease penetrance and other autoimmune traits such as Coombs positive anemia and neurologic deficits. Multiple susceptibility loci of the ancestral strains demonstrate that SLE is inherited as a threshold trait. Because some of these loci co-localize with the susceptibility loci of the insulin-dependent diabetes of nonobese diabetic strain, it is apparent that there are disease-specific as well as autoimmunity-promoting genes. It is proposed that the NZM strains, particularly those with reduced disease penetrance or partial genotypes, provide an improved genetic model for assessment of the effects of environmental agents on SLE and autoimmunity. Images Figure 2 Figure 3 Figure 4

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“…drome by Moritz Kaposi of Vienna in 1872 (1). At the beginning of this century SLE was already believed to be, at least in part, an immune disorder on the basis of observations of false-positive syphilis serology in some patients.…”

Section: The Human Sle Syndromementioning

confidence: 99%

“…Additionally, it was proposed that there are genetic as well as environmental components that contribute to this disease (1,5). Exposure to ultraviolet (UV) radiation, infection, diet, therapeutic drugs, physical and mental stress, and hormonal status (preg?…”

Section: The Human Sle Syndromementioning

confidence: 99%

New Zealand Mixed Mice: A Genetic Systemic Lupus Erythematosus Model for Assessing Environmental Effects

Rudofsky¹,

Lawrence²

1999

Environmental Health Perspectives

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Systemic lupus erythematosus (SLE) is a multiphenotypic autoimmune disease. The hallmark of SLE is the production of anti-double-stranded DNA autoantibodies and the deposition of immune complexes in target tissues such as the kidney, skin, and brain. Additional phenotypic traits are the presence of arthritis, anemia, central nervous system involvement, and a variety of autoantibodies. Females of childbearing age are particularly at risk. Recent genetic analysis of murine SLE shows that susceptibility is under complex polygenic control. It is also apparent that environmental factors contribute to the induction and exacerbation of SLE. We describe here the genotypic and phenotypic characterization of a group of recombinant inbred strains of SLE-prone mice that were derived from NZB and NZW progenitors, the parental strains of the classic female F1 hybrid lupus model. Recombination and reassortment of these ancestral genomes resulted in the NZM (New Zealand mixed) strains with strain-specific patterns of renal disease penetrance and other autoimmune traits such as Coombs positive anemia and neurologic deficits. Multiple susceptibility loci of the ancestral strains demonstrate that SLE is inherited as a threshold trait. Because some of these loci co-localize with the susceptibility loci of the insulin-dependent diabetes of nonobese diabetic strain, it is apparent that there are disease-specific as well as autoimmunity-promoting genes. It is proposed that the NZM strains, particularly those with reduced disease penetrance or partial genotypes, provide an improved genetic model for assessment of the effects of environmental agents on SLE and autoimmunity.

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Description of Systemic Lupus Erythematosus: A Historical Perspective

Cited by 5 publications

References 19 publications

Presence of antibodies to ubiquitin during the autoimmune response associated with systemic lupus erythematosus.

Presence of antibodies to ubiquitin during the autoimmune response associated with systemic lupus erythematosus.

New Zealand mixed mice: a genetic systemic lupus erythematosus model for assessing environmental effects.

New Zealand Mixed Mice: A Genetic Systemic Lupus Erythematosus Model for Assessing Environmental Effects

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