Immunological Relationship between Streptococcus A Polysaccharide and the Structural Glycoproteins of Heart Valve

Goldstein, I.; Halpern, B; Robert, L.

doi:10.1038/213044a0

Cited by 166 publications

(52 citation statements)

References 6 publications

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“…It has also been shown that cross-reactive human and murine monoclonal antibodies recognized N-acetylglucosamine (GlcNAc) of GAS (30,31). GlcNac is the immunodominant cell wall antigen of GAS and has been demonstrated to share crossreactive epitopes with valvular tissue proteins (17) such as myosin, tropomyosin, keratin, vimentin, and laminin (1,6,7,11,24). Furthermore, an anti-GlcNAc/antimyosin monoclonal antibody from a rheumatic carditis patient was shown to be cytotoxic for human endothelial cell lines and also reacted with human valvular endothelium and the underlying basement membrane (14).…”

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confidence: 99%

Association of Mannose-Binding Lectin Gene Polymorphism but Not of Mannose-Binding Serine Protease 2 with Chronic Severe Aortic Regurgitation of Rheumatic Etiology

Ramasawmy

Spina

Faé

et al. 2008

Clin Vaccine Immunol

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N-Acetylglucosamine (GlcNAc) is the major immunoepitope of group A streptococcal cell wall carbohydrates. Antistreptococcal antibodies cross-reactive with anti-GlcNAc and laminin are present in sera of patients with rheumatic fever. The cross-reactivity of these antibodies with human heart valvular endothelium and the underlying basement membrane has been suggested to be a possible cause of immune-mediated valve lesion. Mannose-binding lectin (MBL) encoded by the MBL2 gene, a soluble pathogen recognition receptor, has high affinity for GlcNAc. We postulated that mutations in exon 1 of the MBL2 gene associated with a deficient serum level of MBL may contribute to chronic severe aortic regurgitation (AR) of rheumatic etiology. We studied 90 patients with severe chronic AR of rheumatic etiology and 281 healthy controls (HC) for the variants of the MBL2 gene at codons 52, 54, and 57 by using a PCR-restriction fragment length polymorphism-based method. We observed a significant difference in the prevalence of defective MBL2 alleles between patients with chronic severe AR and HC. Sixteen percent of patients with chronic severe AR were homozygotes or compound heterozygotes for defective MBL alleles in contrast to 5% for HC (P ‫؍‬ 0.0022; odds ratio, 3.5 [95% confidence interval, 1.6 to 7.7]). No association was detected with the variant of the MASP2 gene. Our study suggests that MBL deficiency may contribute to the development of chronic severe AR of rheumatic etiology.Rheumatic fever (RF), which results from a nonsuppurative sequela of pharyngitis caused by group A streptococcus (GAS) in untreated genetically susceptible hosts, displays a wide spectrum of clinical manifestations including carditis, arthritis, chorea, subcutaneous nodules, and erythema marginatum (3). Arthritis occurs in 60 to 65% of patients while carditis, the most serious manifestation and one which often leads to valvular scarring, is observed in 30 to 45% of patients with RF.

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confidence: 99%

Association of Mannose-Binding Lectin Gene Polymorphism but Not of Mannose-Binding Serine Protease 2 with Chronic Severe Aortic Regurgitation of Rheumatic Etiology

Ramasawmy

Spina

Faé

et al. 2008

Clin Vaccine Immunol

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“…Among the cross-reactive antibodies, CHO-Ab is of special interest because, in addition to cross-reactivity with the structural glycoproteins of the human cardiac valves [9,10], it has been reported to persist after an ARF attack only in patients who developed RHD [11][12][13]. The difference, however, could not be confirmed in a large series of patients studied with the agar diffusion precipitation technique [29] rather than the radioimmunoassay.…”

Section: Discussionmentioning

confidence: 89%

“…Since then, multiple crossreactive systems have been reported between streptococcal antigens and human tissues. These included: cross-reactions between the streptococcal cell membrane and the human heart sarcolemmal sheaths [4,5], streptococcal cell membrane and basal ganglia [6], streptococcal M protein and myosin [7], the hyaluronic acid of the streptococcal capsule and the human synovial tissue [8], and the group A specific polysaccharide and the glycopeptides of the heart valves [9,10]. The latter finding was strengthened by the work of other colleagues who reported that elevated levels of the group A specific polysaccharide antibody (CHO-Ab), in the presence of normal titers of antistreptolysin O (ASO) and anti DNA se B, was only maintained in patients with ARF who developed rheumatic heart disease (RHD) [11][12][13].…”

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confidence: 99%

The Group Specific Polysaccharide Antibody in Children with Non-Suppurative Sequelae of Group a Streptococcal Infection

et al. 1993

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; Supported by grant MK015 from the University of Kuwait.; Accepted for publication 9 May 1992.; †Deceased.The kinetics of the group A specific polysaccharide antibody were studied in children with acute rheumatic fever who had no carditis, children with acute rheumatic fever who had carditis and developed rheumatic heart disease and in children with acute poststreptococcal glomerulonephritis. The children with rheumatic fever who had carditis and those who did not, were kept on continuous antistreptococcal prophylaxis. In the group of children who developed rheumatic heart disease the titer of the antibody at onset was significantly higher than those who had rheumatic fever but no carditis (P = 0.01). After a mean follow-up period of three years, a high titer was maintained in children who developed rheumatic heart disease only and was significantly higher than that found in children with rheumatic fever who had no carditis (P = 0.001) and in children with poststreptococcal nephritis (P = 0.001).

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“…This comparison is of particular reflects concentration of antibody binding sites and, interest in view of the suggested relationship between within the range of antibody affinity encountered, is valvular glycoprotein and antibody to the group A carboindependent of K.. This independence contrasts with the hydrate (27), a relationship which raises the possibility results of secondary and tertiary antibody assays in which that high affinity antibody might be removed by adsorpqualitative parameters of antibody such as affinity as-tion to this cross-reactive antigen. Although the present sume great importance (25).…”

Section: Resultsmentioning

confidence: 95%

Qualitative and Quantitative Aspects of the Human Antibody Response to Streptococcal Group A Carbohydrate

Shulman¹,

Ayoub²

1974

J. Clin. Invest.

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Immunological Relationship between Streptococcus A Polysaccharide and the Structural Glycoproteins of Heart Valve

Cited by 166 publications

References 6 publications

Association of Mannose-Binding Lectin Gene Polymorphism but Not of Mannose-Binding Serine Protease 2 with Chronic Severe Aortic Regurgitation of Rheumatic Etiology

Association of Mannose-Binding Lectin Gene Polymorphism but Not of Mannose-Binding Serine Protease 2 with Chronic Severe Aortic Regurgitation of Rheumatic Etiology

The Group Specific Polysaccharide Antibody in Children with Non-Suppurative Sequelae of Group a Streptococcal Infection

Qualitative and Quantitative Aspects of the Human Antibody Response to Streptococcal Group A Carbohydrate

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