| REVIEW ARTICLE |
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| Year : 2020 | Volume
: 15
| Issue : 5 | Page : 13-18 |
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Human leukocyte antigen - HLA B*27: Unraveling the link to pathogenesis
Sakir Ahmed, Ramnath Misra
Department of Clinical Immunology and Rheumatology, Kalinga Institute of Medical Sciences, KIIT University, Bhubaneswar, Odisha, India
Correspondence Address:
Prof. Ramnath Misra
Department of Clinical Immunology and Rheumatology, Kalinga Institute of Medical Sciences, KIIT University, Bhubaneswar - 751 024, Odisha
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0973-3698.284746
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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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