Structural analysis of HLA-B40 epitopes

Kawaguchi, Go; Kato, Noriko; Kashiwase, Kouichi; Karaki, Sachiko; Kohsaka, Takeo; Akaza, Tatsuya; Kano, Kyoichi; Takiguchi, Masafumi

doi:10.1016/0198-8859(93)90125-k

Cited by 23 publications

(6 citation statements)

References 12 publications

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“…[The HLA class I serologic types obtained from the individual carrying a novel allele were A2, 33; B44 (Bw4), blank (Bw6); Cw3.] This result is concordant with the previous reports demonstrated that the relevant B35 serological epitopes were located on the alpha 1 domain (4), while the relevant B40 serologic epitopes resided on the alpha 2 domain (5). These days, hematopoietic stem cell donor banks in worldwide often manage mixed data typed by either serology or DNA method from volunteer donors.…”

supporting

confidence: 91%

A novel hybrid allele (B3563) originated from B350101 and B*4001‐like alleles

Lee¹

2007

Tissue Antigens

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supporting

confidence: 91%

A novel hybrid allele (B3563) originated from B350101 and B*4001‐like alleles

Lee¹

2007

Tissue Antigens

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“…Probably the best characterized and validated association after HLA-B27 is with HLA-B40, most specifically with B:40:01 (a DNA-defined allele that corresponds to HLA-B60 at the serologically defined or protein level) [26]. This association was first described in HLA-B27-positive AS patients from Europe and the USA as far back as 1989 [27], and more recently in the UK and Netherlands [28, 29] HLA-B27-positive patients and in Taiwanese B27-negative patients [30].…”

Section: The Role Of Other Hla Class I and Ii Allelesmentioning

confidence: 99%

An update on the contribution of the MHC to as susceptibility

Reveille

2014

Clin Rheumatol

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The 40-year-old association of HLA-B27 with ankylosing spondylitis is one of the best examples of disease association with a hereditary marker. Genomewide association and family studies suggest that other important major histocompatibility complex (MHC) influences are operative in ankylosing spondylitis (AS) susceptibility. HLA-B27 positive hepatitis C individuals are immunologically more efficient in combating viral infections such as HIV-1, hepatitis C, and influenza and less efficient in combating against certain bacteria (and perhaps other organisms) capable of surviving intracellularly. A recent representative population survey of the frequency of HLA-B27 in the USA found a lower frequency of HLA-B27 in older US adults, perhaps reflecting this. Other HLA class I and class II alleles have been implicated in AS susceptibility, the most consistent being HLA-B*40/B60 (B*40:01) but also B14, B15, A*0201, DRB1*04:04, and certain DPA1 and DPB1 alleles. Non-HLA MHC alleles have also been implicated, although many such studies have been inconsistent, likely due to power issues related to the low number of HLA-B27-negative AS patients examined. The best evidence is for major histocompatibility complex class I chain-related gene A (MICA) whose recognition by intestinal epithelial T cells expressing different V-delta-1 gamma/delta TCR further implicates the gut in AS pathogenesis. The HLA class I and class II and other non-HLA allelic associations underscore the importance of T cells in AS pathogenesis.

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“…Sources of HLA-B molecules were C1R cells transfected Other preferred residues Examples for llgands with the genes for HLA-B58 (B'5801; Ways et al 1985), , HLA-B61 (B'4006; Kawaguchi et al 1993), or HLA-B62 (B'1501; Pola et al 1989). The B62…”

mentioning

confidence: 99%