Association of hla‐b39 with hla‐b27‐negative ankylosing spondylitis and pauciarticular juvenile rheumatoid arthritis in japanese patients

Yamaguchi, Akihiro; Tsuchiya, Naoyuki; Mitsui, Hiroshi; Shiota, M; Ogawa, Atsuko; Tokunaga, Katsushi; Yoshinoya, S; Juji, Takeo; Itō, Kōji

doi:10.1002/art.1780381120

Cited by 126 publications

(78 citation statements)

References 25 publications

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“…Importantly, Cys 67 is a feature that is shared by a relatively small cohort of class I alleles, including subtypes of HLA-B14, -B15, -B38, -B39, and -B73 (49). It is unknown whether these subtypes also form HCdimeric structures, although it is interesting to note that HLA-B39 is also reportedly linked to SpA (50,51). In this report, we have demonstrated that HC-dimer formation can be prevented by replacement of the structural Cys 164 residue.…”

Section: Effect Of Reduced Temperature and Cysmentioning

confidence: 99%

Formation of HLA-B27 Homodimers and Their Relationship to Assembly Kinetics

Antoniou

Ford

Taurog

et al. 2004

Journal of Biological Chemistry

100

143

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The human HLA-B27 class I molecule exhibits a strong association with the inflammatory arthritic disorder ankylosing spondylitis and other related arthropathies. Major histocompatibility complex class I heavy chains normally associate with ␤ 2 -microglobulin and peptide in the endoplasmic reticulum before transit to the cell surface. However, an unusual characteristic of HLA-B27 is its ability to form heavy chain homodimers through an unpaired cysteine at position 67 in the peptide groove. Homodimers have previously been detected within the ER and at the cell surface, but their mechanism of formation and role in disease remain undefined. Here we demonstrate, in the rat C58 thymoma cell line and in human HeLa cells transfected with HLA-B27, that homodimer formation involves not only cysteine at position 67 but also the conserved structural cysteine at position 164. We also show that homodimer formation can be induced in the non-disease-associated HLA class I allele HLA-A2 by slowing its assembly rate by incubation of cells at 26°C, suggesting that homodimer formation in the endoplasmic reticulum may occur as a result of the slower folding kinetics of HLA-B27. Finally, we report an association between unfolded HLA-B27 molecules and immunoglobulin-binding protein at the cell surface.

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Section: Effect Of Reduced Temperature and Cysmentioning

confidence: 99%

Formation of HLA-B27 Homodimers and Their Relationship to Assembly Kinetics

Antoniou

Ford

Taurog

et al. 2004

Journal of Biological Chemistry

100

143

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“…Moreover, from 20 to 30% of patients with ReAdo not have HLA-B27, therefore, B27 is not included in the diagnostic criteria of ReA. Other than HLA-B27,which HLAis attributed to ReA?One possibility is a B27-cross-reacting HLA, that is B7, Bw22, B39, B40, B42 or B60 (3,4). It is important to study HLAtyping in Japanese patients with seronegative spondyloarthropathy (SNSA) since B27 is found in less than 1% in Japan.…”

Section: Hla-b5mentioning

confidence: 99%

Reactive Arthritis or Reiter''s Syndrome and B51-associated Seronegative Spondyloarthropathy

Kobayashi

Ando

2000

Intern. Med.

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“…It has been suggested that certain other HLA-B alleles may also increase susceptibility to AS in B27-negative patients, thus reflecting a degree of heterogeneity in the disease. HLA-B60 has been described as increasing the susceptibility to AS independently of B27 in Caucasians (3), and B39 has been reported to be associated with AS in a B27-negative Japanese population (4). Of interest, some B*39 alleles share striking overlapping peptide repertoires with B27 and may exert an effect on susceptibility to such spondylarthropathies (SpA) as AS and psoriatic arthritis through binding of a potential arthritogenic peptide (5,6).…”

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confidence: 99%

Association of ankylosing spondylitis with HLA–B*1403 in a West African population

López‐Larrea¹,

Mijiyawa²,

González³

et al. 2002

Arthritis & Rheumatism

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Objective. To investigate the contribution of HLA class I alleles in the susceptibility to primary ankylosing spondylitis (AS) in West African patients living in Togo.Methods. A large epidemiologic analysis of 9,065 West African rheumatology patients living in Togo was performed in order to identify those who had AS. Eight Togolese patients with AS were identified. HLA was typed by polymerase chain reaction using sequencespecific oligonucleotide probes. DNA typing was also performed on a control population of 85 healthy subjects matched for ethnic background.Results. A significant association between AS and B*14 was identified. This allele was found in 62.5% of the AS patients (odds ratio 69), but was carried by only 2% of the healthy controls. Analysis for B14 subtypes showed that B*1403 was the predominant allele in AS patients (odds ratio 171), and that this allele was absent in healthy controls. B27 was virtually absent, being observed in only 1 AS patient (B*2705).Conclusion. HLA-B*1403 shows the B27 "supertype" motif and may exert an effect on AS susceptibility according to the arthritogenic peptide model. The association of B*1403 with AS has not previously been reported in either population.

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Association of hla‐b39 with hla‐b27‐negative ankylosing spondylitis and pauciarticular juvenile rheumatoid arthritis in japanese patients

Cited by 126 publications

References 25 publications

Formation of HLA-B27 Homodimers and Their Relationship to Assembly Kinetics

Formation of HLA-B27 Homodimers and Their Relationship to Assembly Kinetics

Reactive Arthritis or Reiter''s Syndrome and B51-associated Seronegative Spondyloarthropathy

Association of ankylosing spondylitis with HLA–B*1403 in a West African population

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