Open AccessHLA‐B27: What is its role in the development of ankylosing spondylitis?
Author(s) -
Cromwell Karen G.,
Baron S. Lynn
Publication year - 1990
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1790030410
Subject(s) - ankylosing spondylitis , hla b27 , human leukocyte antigen , mechanism (biology) , immunology , disease , spondylitis , genetic predisposition , medicine , genetic association , population , antigen , genetics , biology , gene , genotype , environmental health , single nucleotide polymorphism , philosophy , epistemology
Although the association between HLA‐B27 and ankylosing spondylitis (AS) is well established, the mechanism governing this association remains unknown. Although ∼90% of affected individuals possess the HLA‐B27 antigen, HLA‐B27 is also present in ∼8% of the normal population. This article examines the association by reviewing recent literature. Theories proposed have ranged from HLA‐B27's possible role as a marker for an AS susceptibility gene to the possibility of HLA‐B27 being a direct contributor to disease. Theories suggest the presence of pathogenic and benign forms of the antigen, as well as interaction with genetic and environmental factors in disease development. Recent investigations have focused on a link with Klebsiella and its role in a “cross‐reactive” mechanism with HLA‐B27 in AS development. Studies to date have not provided conclusive evidence on the exact mechanism by which HLA‐B27 predisposes individuals to the development of disease. The importance of isolating a specific causative agent for AS is discussed.