Systemic lupus erythematosus: Current state of the genetic hypothesis

Arnett, Frank C.; Reveille, John D.; Wilson, Raymond W.; Provost, Thomas T.; Bias, Wilma Β.

doi:10.1016/0049-0172(84)90006-4

Cited by 83 publications

(26 citation statements)

References 57 publications

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“…An additional part of the background of SLE are genetic factors. The significant concordance (27-57%) for SLE in identical twins (1,2), and the increased frequency of SLE (5-12%) and related immune abnormalities in nonidentical twins and in relatives of SLE patients suggest a genetic influence on the development of SLE (1,(3)(4)(5)(6)(7)(8)(9). Based on these 1.…”

Section: Introductionmentioning

confidence: 99%

“…This RFLP pattern, that is a 1.3-kb and 3.0-kb band pair, was recognized using a complete cDNA probe for the alpha chain, and Pst I digestion of genomic DNA. Furthermore, study of the USA families demonstrated Unrelated American patients 15 16 Multiplex American SLE patients 6 4 Multiplex American SLE relatives 9 11 American controls 4 30 Multiplex Mexican SLE patients 7 15 Multiplex Mexican SLE relatives 8 z s -- [3 can multiplex families and unrelated American patients can be studied. Analysis of nine Mexican families by RFLP using Bgl II and Pst I digestion of genomic DNA and beta and gamma chain probes of the T cell receptor demonstrated no concordance of SLE with any RFLP pattern (data not shown).…”

Section: Introductionmentioning

confidence: 99%

“…These putative genes may be linked to genes that have been found to be increased in frequency in SLE patients: sixth chromosomal markers such as histocompatibility leukocyte antigens (HLA) (e.g., DR2, DR3), and/or C2 and C4 null alleles (3,9,(11)(12)(13)(14)(15), low levels of erythrocyte CR1 receptors (16), and IgG allotypes (17). Suppressor cell defects have also been demonstrated in relatives of SLE patients (7), as have the idiotypic markers of anti-DNA antibodies found in SLE patients (18).…”

Section: Introductionmentioning

confidence: 99%

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Association between a T cell receptor restriction fragment length polymorphism and systemic lupus erythematosus.

Tebib¹,

Alcocer‐Varela²,

Alarcón‐Segovia³

et al. 1990

J. Clin. Invest.

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The present study was designed to test the possibility that T cell receptor genes are associated/linked to those involved in systemic lupus erythematosus (SLE). Genomic DNA was isolated from 31 unrelated Caucasian SLE patients, 34 unrelated Caucasian normals, 5 multiplex American Caucasian SLE families, 9 multiplex Mexican SLE families, and 13 unrelated Mexican normals. The DNA was digested with Pst I, electrophoresed, and transferred to membranes by the Southern blot method. The blots were probed with a cDNA probe for the alpha chain of the T cell receptor. 13 polymorphic RFLP patterns were recognized. 1.3-and 3.0-kb band pairs were observed in 15 of 31 of American Caucasian patients and 4 of 34 American Caucasian controls (chi square, 8.81; P < 0.002; relative risk, 7); there was no association of any RFLP pattern with Mexican SLE. The cDNA probe was cut with Rsa I, EcoR I, and Ava II into fragments corresponding to the V, J, C, and 31UT regions. Only the fragment corresponding to the constant region reacted with the 13/3.0-kb band pair. These observations suggest that a genetic marker of the constant region of the alpha chain of the T cell receptor is associated with genes involved in SLE. (J. Clin. Invest.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Association between a T cell receptor restriction fragment length polymorphism and systemic lupus erythematosus.

Tebib¹,

Alcocer‐Varela²,

Alarcón‐Segovia³

et al. 1990

J. Clin. Invest.

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“…The autoimmune connective tissues diseases systemic lupus erythematosus (SLE) and CREST/PSS (encompassing the two forms of scleroderma: the syndrome of calcinosis, Raynaud's, oesophageal dysfunction, sclerodactyly and telangiectasia, and progressive systemic sclerosis) are diseases in which genetic factors are known to play an important role in determining susceptibility (1), although the aetiology remains unknown. Studies of genetic markers in SLE and CREST/PSS have focused on the major histocompatibility complex, in particular the HLA-DR genes, but reports have failed to be conclusive.…”

Section: Introductionmentioning

confidence: 99%

Gm allogenotype distribution and lack of HLA‐DR, Gm interaction in SLE and CREST/PSS

et al. 1989

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Summary The distribution of Gm allogenotypes (Gm allotypes identified by IgCH restriction fragment length polymorphism (RFLP) analysis) was compared in 66 systemic lupus erythematosus (SLE) patients, 38 CREST/PSS patients and 56 healthy controls. Patient/control comparison showed that Gm homozygosity was increased in the CREST/PSS group (/'<0-05) but not in the SLE group. HLA-DR5 is significantly increased in frequency in this series of CREST/PSS patients compared to controls (f<0-001), and log linear regression analysis showed that although both DR5 and Gm homozygosity were significant factors determining disease susceptibility, there was no evidence of an interactive effect between these two groups of genes increasing the predisposition to CREST/PSS.

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“…The pathogenesis of systemic lupus erythematosus (SLE)' appears to be multifactorial, including both hormonal and environmental influences (1). An important role for a genetic predisposition to SLE has been established by epidemiological analysis and studies of monozygotic twins (2).…”

Section: Introductionmentioning

confidence: 99%

Familial systemic lupus erythematosus. Presence of a cross-reactive idiotype in healthy family members.

Halpern¹,

Davidson²,

Lazo³

et al. 1985

J. Clin. Invest.

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Systemic lupus erythematosus: Current state of the genetic hypothesis

Cited by 83 publications

References 57 publications

Association between a T cell receptor restriction fragment length polymorphism and systemic lupus erythematosus.

Association between a T cell receptor restriction fragment length polymorphism and systemic lupus erythematosus.

Gm allogenotype distribution and lack of HLA‐DR, Gm interaction in SLE and CREST/PSS

Familial systemic lupus erythematosus. Presence of a cross-reactive idiotype in healthy family members.

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