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HLA-B27 Allele (hla-b27 + allele)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Detection of a novel HLA-B27 allele, B*2740, in Taiwanese volunteer bone marrow donors by sequence-based typing: curiosity rewarded

INTERNATIONAL JOURNAL OF IMMUNOGENETICS, Issue 4 2009
M. J. Chen
Summary We report here a novel HLA-B allele, B*2740, discovered in Taiwanese volunteer marrow donors. The new sequence has nucleotide variation at position 527 (T,A) as compared to B*2708. The nucleotide change caused an amino acid substitution from valine (V) to glutamic acid (E) at codon 152. Since B*2740 carries sequence confers to HLA-Bw6 public epitope we believe that this novel B*27 allele might have been generated from a gene conversion involving a Bw4-specific allele (probably B*2704) and a Bw6-specific allele. [source]

1266: Main anterior entities 1: non-granulomatous

ACTA OPHTHALMOLOGICA, Issue 2010
P NERI
Purpose To describe the clinical course, the laboratory work-up and the treatment of different types of anterior non-granulomatous uveitis. Methods The current literature is reviewed and the experience of a tertiary referral centre is reported. Results The lecture describes the most typical subsets of non-granulomatous uveitis. Most part of the talk is dedicated to the most common form of non-granulomatous anterior uveitis: the acute anterior uveitis (AAU), which is very often associated with the HLA-B27 allele. This antigen is also typically associated with the spondyloarthropathies, which are inflammatory joint diseases of the vertebral column. The correct interpretation of the clinical pattern can drive the decision towards the right therapeutic strategy. Other uveitis entities are described also. Conclusion Non-granulomatous uveitis is one of the most important ocular inflammations. It is mandatory to pay attention to the clinical findings and to the laboratory work-up, in order to achieve a good therapeutic approach. [source]

Etiopathogenic role of HLA-B27 alleles in ankylosing spondylitis

INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 3 2005
Nurullah AKKOC
Abstract HLA-B27 is the major genetic susceptibility factor for ankylosing spondylitis (AS). However, its precise role in the pathogenesis of AS still remains unclear, even though its gene has been cloned and sequenced, and its crystallographic structure has been defined. Arthritogenic peptide and molecular mimicry hypotheses propose mechanisms related to an antigen-presenting function of HLA-B27 to be responsible for disease development. However, peculiar aspects of its immunobiology, such as its misfolding and heavy chain dimerization raise the possibility of involvement of pathogenic mechanisms unrelated to its physiological function. Moreover, HLA-B27 is not a single allele, but a family of 31 different alleles, named HLA-B*2701 to HLA-B*2727. Studies worldwide indicate that the relatively common alleles (subtypes) HLA-B*2705, B*2704, and B*2702 are strongly associated with AS, whereas HLA-B*2706 which is prevalent in South-east Asia and HLA-B*2709 which is prevalent on the Italian island of Sardinia, seem to lack such an association. The distinction between the disease-associated subtypes and those that are not associated, may provide clues to the actual role of HLA-B27 in disease pathogenesis. B*2706 differs from B*2704 by only two residues, and B*2709 differs from B*2705 by only one residue. Moreover, both B*2706 and B*2709 bind an endogenous peptide (derived from vasoactive intestinal peptide type 1 receptor) and also an exogenous peptide (latent membrane protein 2 of Epstein-Barr virus) but in two drastically diverse conformations. These recent X-ray diffraction studies of individual peptides in the context of different HLA-B27 alleles broaden our perception of the possible pathogenetic role of this molecule in the development of AS and related spondyloarthopathies. In summary, the pathogenetic role of HLA-B27 in AS seem to be quite heterogenous, and cannot be explained by a single mechanism, and new ideas have been raised based on the aberrant immunobiologic features of HLA-B27. [source]