Human leukocyte antigen - HLA B*27: Unraveling the link to pathogenesis
The association of spondyloarthritis (SpA) with human leukocyte antigen-B*27 (HLA-B*27) is one of the strongest known for a non-monogenic disease. How HLA-B*27 determines the aetiopathogenesis of SpA and disposes toward this group of disease has perplexed rheumatologists for decades. We searched thr...
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| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
SAGE Publishing
2020-01-01
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| Series: | Indian Journal of Rheumatology |
| Subjects: | |
| Online Access: | http://www.indianjrheumatol.com/article.asp?issn=0973-3698;year=2020;volume=15;issue=5;spage=13;epage=18;aulast=Ahmed |
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| Summary: | The association of spondyloarthritis (SpA) with human leukocyte antigen-B*27 (HLA-B*27) is one of the strongest known for a non-monogenic disease. How HLA-B*27 determines the aetiopathogenesis of SpA and disposes toward this group of disease has perplexed rheumatologists for decades. We searched through contemporary bibliographic databases for literature on the link between HLA-B*27 and different SpA, with special emphasis on ankylosing spondylitis. In this review, the structure and function relationship and subtypes of HLA-B*27 are discussed in the context. Then, three hypotheses on the pathological role of HLA-B*27 are presented. The first arthritogenic peptide hypothesis is based on molecular mimicry between the parts of the HLA-B*27 and epitopes of pathogenic Enterobacteriaceae. The second hypothesis is about the misfolding of the HLA-B*27 major chain, leading to endoplasmic reticulum (ER) stress and initiation of inflammation through the unfolded protein response. The third hypothesis deals with the formation of homodimers of the HLA-B*27 major chain on the cell surface, leading to the activation of natural-killer cells through the killer immunoglobulin-like receptors. Furthermore, discussed in the review are the epistatic factors such as ER-associated peptidase-1, role of microbiota, and the concept of autoinflammation in relation to HLA-B*27. |
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| ISSN: | 0973-3698 0973-3701 |