HLA antigens in 88 cases of rheumatic fever observed in Martinique

Monplaisir, N; Valette, Ignez; Bach, Jean‐François

doi:10.1111/j.1399-0039.1986.tb00484.x

Cited by 20 publications

(5 citation statements)

References 6 publications

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“…However, these studies revealed that some common HLA‐DR alleles like HLA‐DR/DQ were a risk factor for RHD, encompassing ethnicity. Our results for DRB1*01 (Monplaisir et al ., 1986; Maharaj et al ., 1987; Donadi et al ., 2000; Shulman & Ayoub, 2002), DRB1*04 (Khosroshahi et al ., 1992; Bhat et al ., 1997; Wani, 1997), DRB1*07 (Ozkan et al ., 1993; Debaz et al ., 1996; Guedez et al ., 1999; Visentainer et al ., 2000; Stanevicha et al ., 2003) and DQB1*02 (Taneja et al ., 1989; Debaz et al ., 1996) are consistent with these findings.…”

Section: Discussionmentioning

confidence: 60%

“…Numerous studies focusing on the relation of HLA alleles with RHD were undertaken without reaching a conclusion (Anastasiou‐Nana et al ., 1986; Ayoub et al ., 1986; Jhinghan et al ., 1986; Monplaisir et al ., 1986; Maharaj et al ., 1987; Rajapakse et al ., 1987; Taneja et al ., 1989; Reddy et al ., 1990; Guilherme et al ., 1991; Khosroshahi et al ., 1992; Olmez et al ., 1993; Ozkan et al ., 1993; Weidebach et al ., 1994; Koyanagi et al ., 1996; Bhat et al ., 1997; Gu et al , 1997; Maharaj et al ., 1997; Wani, 1997; Guedez et al ., 1999; Donadi et al ., 2000; Visentainer et al ., 2000; Pacheco et al ., 2003; Stanevicha et al ., 2003). In our study, a possible association of RHD with HLA‐B13 was detected, but this relation became insignificant when corrected for multiple comparisons.…”

Section: Discussionmentioning

confidence: 99%

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The role of HLA molecules in susceptibility to chronic rheumatic heart disease

Kudat

Telci

Sözen

et al. 2006

Int J Immunogenetics

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Only a small fraction of the streptococcal pharyngitis progress to rheumatic carditis, which implies that environmental, host and microbial factors interact to cause an aberrant immune response against the antigens of the microorganism that cross-react with cardiac tissues. Although there are numerous studies and a general consensus on the relation between human leucocyte antigen (HLA) class II antigens and rheumatic heart disease (RHD), the details and the culprit antigens are still controversial. The study was undertaken to examine 100 patients with chronic RHD and 100 controls for HLA class I and class II antigens for differences in prevalence. All samples were typed at the HLA-DRB1/3/4/5 and DQB1 loci by the sequence-specific primer (PCR-SSP) method at low resolution. For HLA class I antigens, HLA-B13 frequency was marginally increased in patients with RHD compared to controls without reaching statistical significance. For class II antigens, RHD patients had higher frequencies for HLA-DRB1*01 (RHD 24%, controls 10%), DRB1*04 (RHD 35%, controls 26%), DRB1*07 (RHD 18%, controls 11%) and HLA-DQB1*02 (RHD 32%, controls 17%) without reaching statistical significance, and significantly lower frequencies for DRB1*13 (Pc < 0.003, OR: 5.69), DRB5* (Pc < 0.003, OR: 33) and DRB3* (Pc = 0.03, OR: 2.66) compared to controls. It was concluded that host, microbial and environmental factors collude to create acute rheumatic fever (RF) and chronic rheumatic valve disease. The HLA-DRB1*13, DRB5* and DRB3* were protective against the development of rheumatic valve damage.

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Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 99%

The role of HLA molecules in susceptibility to chronic rheumatic heart disease

Kudat

Telci

Sözen

et al. 2006

Int J Immunogenetics

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“…HLA-DR4 and DR9 were found to be associated with RF also in American Caucasians, Arabians, and in Indians from Kashmir [10,11,12,13]. Other HLA class II antigens such as DR1, DR2, DR3, and DR6 were also found to be associated with RF/RHD in other populations [11,[14][15][16][17][18]. In Japanese RHD patients, susceptibility to mitral stenosis seems to be in part controlled by one or more genes in the HLA-DQ region, in close linkage disequilibrium with HLA-DQA*0104 and DQB1*05031 [19].…”

Section: Host Genetic Factorsmentioning

confidence: 94%

“…Peptides M5(81-96) and M5(91-103) were recognized by 46.0% of severe RHD patients and 8.6% of healthy subjects (P=0.0005), and 24.3% of severe RHD and 3.0% of healthy subjects (P=0.01), respectively ( Table 1) [43]. Peptides M5 (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25) and M5(125-139) were preferentially recognized by mild RHD patients when compared to healthy subjects (P=0.008 and P=0.01), respectively ( Table 1). Reactivity to peptide M5(101-120) discriminates between severe and mild RHD patients (P=0.03).…”

Section: Cellular Immune Responsementioning

confidence: 98%

T Cell Response in Rheumatic Fever: Crossreactivity Between Streptococcal M Protein Peptides and Heart Tissue Proteins

Guilherme

Faé²,

Oshiro³

et al. 2007

CPPS

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Molecular mimicry between streptococcal and human proteins has been proposed as the triggering factor leading to autoimmunity in rheumatic fever (RF) and rheumatic heart disease (RHD). In this review we focus on the studies on genetic susceptibility markers involved in the development of RF/RHD and molecular mimicry mediated by T cell responses of RHD patients against streptococcal antigens and human tissue proteins. We identified several M protein epitopes recognized by peripheral T cells of RF/RHD patients and by heart tissue infiltrating T cell clones of severe RHD patients. The regions of the M protein preferentially recognized by human T cells were also recognized by murine T cells. By analyzing the T cell receptor (TCR) we observed that some Vbeta families detected on the periphery were oligoclonal expanded in the heart lesions. These results allowed us to confirm the major role of T cells in the development of RHD lesions.

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“…HLA‐DR7 was also found in other populations, such as Turkish [28, 29], Latvian (in which the association of HLA‐DRB1*07 and DQB1*0302 or DQB1*0401‐2 was also associated with the development of valvular lesions [30]), and also in RHD patients from Northern Egypt with severe mitral valve disease [31] (Table 1). Other HLA class II alleles (HLA‐DR and HLA‐DQ) were also found in association with RF/RHD in different populations [32–39] as shown in Table 1. The strength of correlation of HLA class II alleles ranges from 2.3 times to 13.6 (RR = 2.3–13.6) (Table 1) indicating that these alleles play a key role in the development of the disease.…”

Section: Genetic Influence Of the Major Histocompatibilty Complexmentioning

confidence: 99%

Rheumatic Fever and Rheumatic Heart Disease: Genetics and Pathogenesis

2007

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Molecular mimicry between streptococcal and human proteins is considered as the triggering factor leading to autoimmunity in rheumatic fever (RF) and rheumatic heart disease (RHD). Here, we present a review of the genetic susceptibility markers involved in the development of RF/RHD and the major immunopathological events underlying the pathogenesis of RF and RHD. Several human leucocyte antigen (HLA) class II alleles are associated with the disease. Among these alleles, HLA‐DR7 is predominantly observed in different ethnicities and is associated with the development of valvular lesions in RHD patients. Cardiac myosin is one of the major autoantigens involved in rheumatic heart lesions and several peptides from the LMM (light meromyosin) region were recognized by peripheral and intralesional T‐cell clones from RF and RHD patients. The production of TNF‐α and IFN‐γ from heart‐infiltrating mononuclear cells suggests that Th‐1 type cytokines are the mediators of RHD heart lesions while the presence of few interleukin‐4 producing cells in the valve tissue contributes to the maintenance and progression of the valvular lesions.

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HLA antigens in 88 cases of rheumatic fever observed in Martinique

Cited by 20 publications

References 6 publications

The role of HLA molecules in susceptibility to chronic rheumatic heart disease

The role of HLA molecules in susceptibility to chronic rheumatic heart disease

T Cell Response in Rheumatic Fever: Crossreactivity Between Streptococcal M Protein Peptides and Heart Tissue Proteins

Rheumatic Fever and Rheumatic Heart Disease: Genetics and Pathogenesis

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