Lack of association of HLA‐DR antigens with progressive systemic sclerosis (scleroderma)

Nikš, M; Rovenský, Jozef; Nyulassy, S; Buc, Milan; Stefanovic, J; Zitnan, D

doi:10.1111/j.1399-0039.1982.tb01446.x

Cited by 15 publications

(5 citation statements)

References 2 publications

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“…Since we also looked at several other Gm allotypic markers separately (Gml, 2, and 3), the P value used for the Gm(23) comparison must be multiplied by 4; when this is done, the P value is no longer found to be significant. In whites, Gm (17) and Gm(21) are almost always found with Gm(l), while Gm(5) and Gm (13) …”

Section: Immunoglobulin Allotypesmentioning

confidence: 99%

Anticentromere Antibody and Immunoglobulin Allotypes in Scleroderma

Chen¹

1985

Arch Dermatol

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Section: Immunoglobulin Allotypesmentioning

confidence: 99%

Anticentromere Antibody and Immunoglobulin Allotypes in Scleroderma

Chen¹

1985

Arch Dermatol

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“…However, these HLA associations were not strong and were sometimes inconsistent with each other. In some studies, no significant association was found (22)(23)(24).…”

Section: Introductionmentioning

confidence: 99%

The HLA-DR and DQ genes control the autoimmune response to DNA topoisomerase I in systemic sclerosis (scleroderma).

Kuwana¹,

Kaburaki²,

Okano³

et al. 1993

J. Clin. Invest.

102

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HLA class II alleles were determined using the PCR-RFLP method in Japanese systemic sclerosis (scleroderma) patients with (n = 28) or without (n = 34) anti-topoisomerase I antibodies (anti-topo I). Either the DQB1 *0601 or * 0301 allele was recognized in all anti-topo I positive patients, compared with 44% of anti-topo I negative patients (P < 0.00001, relative risk[RR] > 41) or 58% of Japanese healthy control subjects (P < 0.00001, RR > 24). Tyrosine at position 26 in the second hypervariable region in the ,81 domain of the DQB1 gene is common to these two alleles and is not present in any other known DQB1 alleles. We also examined immunoreactivities of anti-topo I positive sera to four different autoantigenic B cell epitopes of topo I molecule that were expressed as recombinant fusion proteins. One major B cell epitope, located within the region corresponding to amino acid residues 74-248, was perfectly associated with the amino acid sequence FLEDR at positions 67-71 in the j1 domain of the DRB gene. Two other epitopes, corresponding to 316-441 or 658-700, were associated with the serologically defined HLA-DR52 antigen. Patients with both FLEDR and DR52 demonstrated higher antitopo I antibody titers. These results suggest that the HLA-DR and DQ genes together control the autoimmune response to topo I in systemic sclerosis. (J. Clin. Invest. 1993. 92:1296-1301

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“…A number of studies have reported associations of HLA antigens with PSS, including MHC class I specificities: HLA-A9 (8,9), B8 (10,11 ), and B35 (12,13); MHC class II specificities: HLA-DR 1 (13)(14)(15)(16), DR3 (ll,17), and DR5 (16,(18)(19)(20); and MHC class III specificities: C4 null alleles (12,19). These associations have varied among different centers, with some groups unable to show any HLA associations with PSS (21)(22)(23)(24)(25).…”

Section: Introductionmentioning

confidence: 99%

Association of amino acid sequences in the HLA-DQB1 first domain with antitopoisomerase I autoantibody response in scleroderma (progressive systemic sclerosis).

Reveille¹,

Durban²,

Clair³

et al. 1992

J. Clin. Invest.

132

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Previous studies in Caucasians with progressive systemic sclerosis (PSS) have suggested associations of antitopoisomerase I (antitopo I) autoantibodies with either serologically defined HLA-DR2 or DR5. To better define class II HLA associations with the antitopo I response, 161 PSS patients (132 Caucasians and 29 American blacks) were studied for antitopo I autoantibodies by immunodiffusion and immunoblotting, and their HLA-DRB1, DRB3, DQA1, and DQB1 alleles were determined by restriction fragment length polymorphic analysis and DNA oligotyping. Among Caucasians with antitopo I, HLA-DR5(DRB1*1101-*1104), DRB3*0202 and DQw3 (DQw7,8,9) were significantly increased in frequency. In American blacks, however, only HLA-DQB1 *0301 (DQw7) was significantly increased. The presence of HLA-DQB1 *0301 (DQw7) and other HLA-DQB1 alleles bearing the uncharged polar amino acid residue tyrosine at position 30 of the outermost domain was found in all antitopo I-positive Caucasian PSS patients compared with 66% of antitopo I-negative PSS patients (pc = 0.007) and 70% of normal controls (pc = 0.008), as well as all antitopo I-positive black patients. The association with HLA-DQB1 was independent of HLA-DR5(DRB1*1101-*1 104) or any other HLA-DRB1, DRB3, or DQA1 alleles. Alternative or additional candidate epitopes for this autoimmune response include alanine at position 38 and threonine at position 77 of these same DQB1 alleles. These data suggest that genetic predisposition to the antitopo I response in PSS is associated most closely with the HLA-DQB1 locus. (J. Clin. Invest. 1992. 90:973-980.)

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Lack of association of HLA‐DR antigens with progressive systemic sclerosis (scleroderma)

Cited by 15 publications

References 2 publications

Anticentromere Antibody and Immunoglobulin Allotypes in Scleroderma

Anticentromere Antibody and Immunoglobulin Allotypes in Scleroderma

The HLA-DR and DQ genes control the autoimmune response to DNA topoisomerase I in systemic sclerosis (scleroderma).

Association of amino acid sequences in the HLA-DQB1 first domain with antitopoisomerase I autoantibody response in scleroderma (progressive systemic sclerosis).

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