HLA-DR1 and DRw6 association in DR4-negative rheumatoid arthritis patients

Läng, B; Melchers, Inga; Urlacher, A.; Tanzi-Fetta, R. F.; Kohlbrenner, S; Tongio, M. M.; Peter, Hans‐Hartmut

doi:10.1007/bf02274843

Cited by 25 publications

(7 citation statements)

References 45 publications

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“…1), as well as HLA–DR3 (where *0301 is the major subtype associated) in Kuwait (11, 21). Furthermore, protective effects were reported for DRB1*07 (3, 13, 22–25), *1201 (26), *1301 (24, 26–28), and *1501 (29, 30). Multivariate logistic regression analysis was performed using the SPSSX package (SPSS, Chicago, IL).…”

Section: Methodsmentioning

confidence: 99%

Reshaping the shared epitope hypothesis: HLA‐associated risk for rheumatoid arthritis is encoded by amino acid substitutions at positions 67–74 of the HLA–DRB1 molecule

Vries¹,

Tijssen²,

Riel³

et al. 2002

Arthritis & Rheumatism

115

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Objective To further analyze the association of HLA–DRB1 alleles with disease susceptibility in recent‐onset rheumatoid arthritis (RA). Methods One hundred sixty‐seven Caucasian RA patients and 166 healthy controls were typed for HLA–DRB1. Results The association of susceptibility to RA with the group of alleles encoding the shared epitope susceptibility sequences (SESSs) was confirmed in recent‐onset RA. Among non‐SESS alleles, DRB1*07, *1201, *1301, and *1501 showed significant protective effects. Even after correction for the influence of SESS alleles, significant independent protective effects of DRB1 alleles were observed. Protective alleles shared a third hypervariable region motif. Independent homozygosity effects were observed both for susceptibility and for protective alleles. Conclusion Nonsusceptibility alleles differ significantly with regard to RA risk. Protective alleles show clear homology at positions 67–74, often encoding isoleucine at position 67 or aspartic acid at position 70. Susceptibility and protective alleles both show homozygosity effects. Based on these results and on data reported in the literature, in order to incorporate the finding of differential risks among nonsusceptibility alleles, we propose to reshape the shared epitope hypothesis as follows: HLA‐associated risk for RA is encoded by amino acid substitutions at positions 67–74 of the HLA–DRB1 molecule.

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Section: Methodsmentioning

confidence: 99%

Reshaping the shared epitope hypothesis: HLA‐associated risk for rheumatoid arthritis is encoded by amino acid substitutions at positions 67–74 of the HLA–DRB1 molecule

Vries¹,

Tijssen²,

Riel³

et al. 2002

Arthritis & Rheumatism

115

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“…He was treated with oral gold salts, prednison (5 mg/day) and non-steroidal anti-inflammatory drugs, but received no immunosuppressive therapy. The result of human leucocyte antigen (HLA) typing by serological methods and by sequencing HLA-DRB genes amplified by polymerase chain reaction was: A2, B5, B60, DR4w4, DRw13(6)-Dw19, DRw52c, DQwl, DQw3 [24,25]. PTW underwent arthroscopic synovectomy-a technique giving rise to a cell suspension immediately after the operation, without further manipulation.…”

Section: Methodsmentioning

confidence: 99%

Reactivity Patterns of Synovial T‐Cell Lines Derived from a Patient with Rheumatoid Arthritis. I. Reactions with Defined Antigens and Auto‐Antigens Suggest the Existence of Multireactive T‐Cell Clones

Melchers

Jooss-Rüdiger

1997

Scand J Immunol

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The functional T-cell repertoire in the inflamed joint of a patient with rheumatoid arthritis was analysed at the clonal level. Using limiting dilution techniques and selecting for growth of in vivo activated and/or autoreactive T cells, 149 T-cell lines were established. They were tested in a proliferation assay for reactivity against an autologous Epstein-Barr virus (EBV)-transformed B-cell line and a panel of auto-antigens and foreign antigens. Seventy-five lines (ϳ50%) could be stimulated. Thirty-six lines (ϳ24%) were antigenreactive. They were stimulated by human collagens type I (15), II (10), IV (7) or V (4), cartilage proteoglycans (4), Mycobacterium tuberculosis (15), the 60 kDa heat-shock protein of M. bovis (13) or tetanus toxoid (10). T-cell lines were either monoreactive (19), bireactive (6), or multireactive (11), i.e. they were stimulated by either one, by two, or by more antigens in the panel. About half of the antigen-reactive lines were at the same time autoreactive towards the autologous B-cell line. These data suggest the existence of multispecific autoreactive T-cell receptors comparable to multireactive or natural autoantibodies and prove the presence of autoantigen-reactive T cells in the inflamed joints of patients with rheumatoid arthritis.

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“…Protective alleles operate conspicuously in insulin-dependent diabetes melitus (IDDM), where certain HLA-DQ alleles associated with HLA-DR2 show this type of negative association with disease (Thomson et al 1988;Baisch et al_ 1990;Zeliszewski et al 1992;Kockum et al 1993). In rheumatoid arthritis (RA), negative association has been found for HLA-DR2 (Jarequemada et al 1986;Ollier et al 1986;Stasny et al 1988;Mehra et al 1993), HLA-DR5 (Jarequemada et al_ 1986; Lang et al 1990), and HLA-DR7 haplotypes (Jarequemada et al 1986;Walker et al 1986), although the latter observation has not been confirmed in N. Avrion Mitchison (~) • Monika C. Brunner Deutsches Rheuma-Forschungszentrum, Nordufer 20, D-13353 Berlin, Germany other studies (Rigby et al 1991). HLA-DR7 (DRBI*07) is protective in early onset pauciarticular juvenile chronic arthritis (Paul et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Association of H2A b with resistance to collagen-induced arthritis in H2-recombinant mouse strains: an allele associated with reduction of several apparently unrelated responses

Mitchison

Brunner

1995

Immunogenetics

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HLA class II alleles can protect against immunological diseases. Seeking an animal model for a naturally occurring protective allele, we screened a panel of H2-congenic and recombinant mouse strains for ability to protect against collagen-induced arthritis. The strains were crossed with the susceptible strain DBA/1, and the F1 hybrids immunized with cattle and chicken type II collagen. Hybrids having the H2Ab allele displayed a reduced incidence and duration of the disease. They also had a reduced level of pre-disease inflammation, but not of anti-collagen antibodies. The allele is already known to be associated with reduction of other apparently unrelated immune responses, suggesting that some form of functional differentiation may operate that is not exclusively related to epitope-binding. It is suggested that this may reflect allelic variation in the class II major histocompatibility complex promoter region.

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HLA-DR1 and DRw6 association in DR4-negative rheumatoid arthritis patients

Cited by 25 publications

References 45 publications

Reshaping the shared epitope hypothesis: HLA‐associated risk for rheumatoid arthritis is encoded by amino acid substitutions at positions 67–74 of the HLA–DRB1 molecule

Reshaping the shared epitope hypothesis: HLA‐associated risk for rheumatoid arthritis is encoded by amino acid substitutions at positions 67–74 of the HLA–DRB1 molecule

Reactivity Patterns of Synovial T‐Cell Lines Derived from a Patient with Rheumatoid Arthritis. I. Reactions with Defined Antigens and Auto‐Antigens Suggest the Existence of Multireactive T‐Cell Clones

Association of H2A b with resistance to collagen-induced arthritis in H2-recombinant mouse strains: an allele associated with reduction of several apparently unrelated responses

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