attomol^® HLA-B*27

Human leukocyte antigen B (HLA-B) is a glycoprotein in the major histocompatibility complex (MHC), which is expressed on almost all nucleated somatic cells and is encoded on the short arm of chromosome 6 [1]. Human leukocyte antigens present endogenous antigens to cytotoxic T cells and are partly responsible for the immunological individuality of humans (recognition of ‘endogenous’ and ‘exogenous’) [1]. Different forms of HLA-B antigens exist, which are called determinants (e.g., HLA-B*7, -B*8, -B*15). One of these determinants, HLA-B*27, was closely associated with rheumatic diseases, particularly ankylosing spondylitis (AS, also known as Morbus Bechterew), as early as 1973 [2]. Men have a higher risk of developing AS and disease onset is typically expected between the ages of 20 and 40 years [1]. Althrough AS has also been identified in a small number of patients without the HLA-B*27 allele, the HLA-B*27 antigen has been found in 90 % of individuals with AS and is thus considered the most important factor in the detection of AS [3][4]. Until now, HLA-B*27 was detected serologically. Recently, this method is increasingly replaced by molecular biological techniques, because molecular tests work without living cells and are cheaper and easier to perform. The genetic determination of the HLA-B27 allele is considered useful for patients under 45 years who have back pain lasting longer than 3 months. The disease onset is typical between age 20 and 40. An early stage diagnosis is necessary so that patients benefit from timely therapy [5]. The genetic determination of the HLA-B*27 allele is not considered useful according to AWMF guidelines if other criteria speak against the presence of axial spondyarthritis. These include missing hints on imaging procedures, absence of inflammatory back pain, and age of manifestation > 45 years [6].

Prevalence
The presence of the HLA-B*27 allele represents a significant congenital risk factor for ankylosing spondylitis with a global prevalence of approx. 0.1-1.4 % in various samples [6][7]. The prevalence appears to vary widely geographically. The carriers of HLA-B*27 have an 87 times higher risk of developing spondyloarthritis (SpA) than carriers of other HLA-B determinants. HLA-B*27 occurs in about 7 % of the Western European population. In patients with ankylosing spondylitis, however, it occurs in 80-90 % [8].

[1] Parameswaran P, Lucke M.: HLA B27 Syndromes. Treasure Island (FL): StatPearls Publishing, 2020.
[2] Brewerton D. A. et al.: Ankylosing spondylitis and HL-A 27. Lancet, 1973, 1(7809), 904-7.
[3] Chen B. et al: Role of HLA-B27 in the pathogenesis of ankylosing spondylitis (Review). Molecular Medicine Reports 15, 2017, 1943-1951.
[4] Bowness P.: HLA-B27. Annual Review of Immunology, 2015, 33:29-48.
[5] Van den Berg, R. et al.: How should we diagnose spondyloarthritis according to the ASAS classification criteria. Polskie Archiwum Medycyny Wewnethznej, 2010, 120 (11):452-457.
[6] Evidenzbasierte Leitlinie der Deutschen Gesellschaft für Rheumatologie (DGRh) und der beteiligten medizinisch-wissenschaftlichen Fachgesellschaften und weiterer Organisationen: Axiale Spondyloarthritis inklusive Morbus Bechterew und Frühformen. Langfassung,. AWMF-Leitlinien Register Nummer: 060/003, Entwicklungsstufe S3, Version: 2019.
[7] Dean L. E. et al.: Global prevalence of ankylosing spondylitis. Rheumatology, 2014, 53(4): 650-57.
[8] Isselbacher et al.: Harrisons Innere Medizin 1. 1995, 13. Auflage, Blackwell-Wissenschaftsverlag, S. 453-460

• PCR-H₂O
• PCR-buffer III
• primer HLA-B*27
• instructions for use

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