The role of HLA-B*27 in spondyloarthritis

Robert A. Colbert, Fatemeh Navid, Tejpal Gill

Research output: Contribution to journalReview articlepeer-review

30 Scopus citations


The mechanism by which HLA-B*27 predisposes to spondyloarthritis remains unresolved. Arthritogenic peptides have not been defined in humans and are not involved in experimental models of spondyloarthritis. Aberrant properties of HLA-B*27 can activate the IL-23/IL-17 axis in HLA-B*27 transgenic rats and humans. In HLA-B*27-independent rodent models, spondyloarthritis can be driven by IL-23 triggering entheseal-resident CD4-/CD8- T cells or CD4+ Th17 T cells. These findings point toward noncanonical mechanisms linking HLA-B*27 to the disease and provide a potential explanation for HLA-B*27-negative spondyloarthritis. Gut microbial dysbiosis may be important in the development of spondyloarthritis. HLA-B*27-induced changes in gut microbiota are complex and suggest an ecological model of dysbiosis in rodents. The importance of the IL-23/IL-17 axis in ankylosing spondylitis has been demonstrated by studies showing efficacy of IL-17. Although deciphering the precise role(s) of HLA-B*27 in disease requires further investigation, considerable progress has been made in understanding this complex relationship.

Original languageEnglish (US)
Pages (from-to)797-815
Number of pages19
JournalBest Practice and Research: Clinical Rheumatology
Issue number6
StatePublished - Dec 2017
Externally publishedYes


  • Ankylosing spondylitis
  • Arthritogenic peptides
  • Autophagy
  • Dysbiosis
  • Endoplasmic reticulum-associated aminopeptidase-1 (ERAP1)
  • Endoplasmic reticulum-associated degradation (ERAD)
  • Inflammatory bowel disease
  • Microbiota
  • Protein misfolding
  • Spondyloarthritis

ASJC Scopus subject areas

  • Rheumatology


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