Ro and La antigens and maternal anti-La idiotype on the surface of myocardial fibres in congenital heart block

Horsfall, Angela C.; Venables, P. J. W.; Taylor, Pamela V.; Maini, R. N.

doi:10.1016/0896-8411(91)90015-5

Cited by 110 publications

(37 citation statements)

References 18 publications

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“…HLA-DRB1*03011 and the haplotype DR3;DQ2, in fact, seemed not to be the primary disease-associated genes for CCHB in a child, but were instead associated with or involved in a strong SS-like anti-Ro/La response. On the other hand, anti-Ro/La antibodies, and in particular anti-52-kd, have been claimed to have a direct pathogenic role in the development of CCHB (3,(5)(6)(7)(8)46). What makes these antibodies pathogenic or what preferentially elicits an anti-52-kd response remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Many reports agree that high titers of anti-52-kd Ro and/or anti-48-kd La autoantibodies in mothers' sera are a major risk for CCHB in their offspring (2)(3)(4)(5), since the antibodies are thought to have a direct pathogenic role. Anti-Ro/SSA and/or anti-La/SSB antibodies cross the placenta after the sixteenth week of gestation, bind to autoantigens in the developing fetal heart, and possibly, elicit an inflammatory tissue injury (6)(7)(8). This profile of anti-Ro/La response is not unique to the mothers of children with CCHB (4,9).…”

mentioning

confidence: 90%

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DNA typing of maternal HLA in congenital complete heart block: Comparison with systemic lupus erythematosus and primary Sj�gren's syndrome

Colombo

Brucato

Coluccio

et al. 1999

Arthritis & Rheumatism

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Objective. To investigate which maternal HLA allele or haplotype is primarily associated with isolated congenital complete heart block (CCHB) in offspring.Methods. HLA class II typings were assessed by line probe assay and polymerase chain reactionsequence-specific oligonucleotide probe methods, and HLA class I by the microlymphocytotoxicity test, in 13 Results. HLA-DRB1*03011 and DRB1*03011; DQA1*0501;DQB1*0201 were more frequent in mothers of infants with CCHB than in mothers who had SLE, but not in mothers who had SS and whose children were healthy. Mothers of infants with CCHB were either HLA-B5/35, B17, or B44 positive and had a higher prevalence of B44;DRB11;DQA1*0501;DQB1*0301 and isolated anti-52-kd antibodies, which were absent in SS and SLE controls.Conclusion. Mothers of infants with CCHB presented a strong genetic similarity to mothers who had SS, except for HLA class I phenotype. HLA-DRB1*03011;DQA1*0501;DQB1*0201 seemed not to be primary CCHB-associated genes, but were involved in an SS-like anti-Ro/La response. The combined presence of HLA-DRB1*03011 and anti-52-kd SSA/Ro antibodies conveyed the highest risk of giving birth to an affected child.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 90%

DNA typing of maternal HLA in congenital complete heart block: Comparison with systemic lupus erythematosus and primary Sj�gren's syndrome

Colombo

Brucato

Coluccio

et al. 1999

Arthritis & Rheumatism

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“…Indeed, the role of anti-Ro/SSA and/or anti-La/SSB in CHB is not clear. It has been suggested that these antibodies react with their corresponding antigens on the surface of the cells of the conduction system in the heart (Horsfall et al 1991). Although antiRo/SSA antibodies have been eluted from affected fetal cardiac tissue (Reichlin et al 1994), there is no reason to expect the expression of the Ro/SSA protein, a nucleoprotein, in the surface membrane of the cardiac cells.…”

Section: The Neonatal Lupus Syndromementioning

confidence: 96%

Neonatal lupus syndrome: the heart as a target of the immune system

Garcia

Carvalho

2000

An. Acad. Bras. Ciênc.

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Neonatal lupus erythematosus (NLE) is an auto-immune disease related to systemic lupus erythematosus (SLE). Unlike SLE it is not a spontaneous syndrome but rather an acquired one. In NLE the most common disease manifestations are a transient cutaneous lesion and cardiac conduction disturbances. The cutaneous lesions and other non-cardiac manifestations of NLE are transient and disappear about six months after birth, at the time when maternal antibodies disappear from the neonatal circulation. This fact suggests that maternal antibodies may cross the placenta leading to an inflamatory reaction in the fetal tissues. NLE is the principal cause of atria-ventricular block, when it is not associated with congenital birth defects. All the clinical studies to date correlate the heart block in NLE with the presence of certain types of circulating maternal antibodies, against the Ro/SSA nuclear proteins, in the serum of the newborn. In this paper we discuss animal models that have been developed by our and others groups to study the participation of the anti-Ro/SSA antibodies in the pathogenesis of the cardiac conduction blockades that occur in NLE.

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“…Although proof of pathogenicity is not definitive, accumulating evidence suggests that anti-SS-A/Ro antibodies contribute to the cardiac and tissue damage in NLE (4,(35)(36)(37). A molecular definition of the SS-A/Ro autoantigens has been provided by the cloning of cDNAs, but little is known about their biologic function other than binding to hY RNAs or their role in disease pathogenesis and tissue injury.…”

Section: Discussionmentioning

confidence: 99%

Defining a novel 75-kDa phosphoprotein associated with SS-A/Ro and identification of distinct human autoantibodies

Wang¹,

Buyon²,

Zhu³

et al. 1999

J. Clin. Invest.

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Ro and La antigens and maternal anti-La idiotype on the surface of myocardial fibres in congenital heart block

Cited by 110 publications

References 18 publications

DNA typing of maternal HLA in congenital complete heart block: Comparison with systemic lupus erythematosus and primary Sj�gren's syndrome

DNA typing of maternal HLA in congenital complete heart block: Comparison with systemic lupus erythematosus and primary Sj�gren's syndrome

Neonatal lupus syndrome: the heart as a target of the immune system

Defining a novel 75-kDa phosphoprotein associated with SS-A/Ro and identification of distinct human autoantibodies

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