Abstract
The human major histocompatibility complex (MHC) class I gene, HLA-B27, is a strong risk factor for susceptibility to a group of disorders termed spondyloarthropathies. Rodents that express HLA-B27 develop spondyloarthropathies, implicating HLA-B27 in the etiology of these disorders. To determine whether an HLA-B27-like molecule was associated with spondyloarthropathies in nonhuman primates, we analyzed the MHC class I cDNAs expressed in a cohort of rhesus macaques that developed reactive arthritis after an outbreak of shigellosis. We identified several cDNAs with only limited sequence similarity to HLA-B27. Interestingly, one of these MHC molecules had a B pocket identical to that of HLA-B39. Pool sequencing of radiolabeled peptides bound by this molecule demonstrated that, like HLA-B27 and HLA-B39, it could bind peptides with arginine at the second position. However, extensive analysis of the MHC class I molecules in this cohort revealed no statistically significant association between any particular MHC class I allele and susceptibility to reactive arthritis. Furthermore, none of the rhesus MHC class I molecules bore a strong resemblance to HLA-B27, indicating that reactive arthritis can develop in this animal model in the absence of an HLA-B27-like molecule. Surprisingly, there was a statistically significant association between the rhesus macaque MHC locus allele, Mamu-A*12, and the absence of reactive arthritis following Shigella infection.
Original language | English (US) |
---|---|
Pages (from-to) | 314-325 |
Number of pages | 12 |
Journal | Immunogenetics |
Volume | 51 |
Issue number | 4-5 |
DOIs | |
State | Published - 2000 |
Keywords
- Autoimmunity
- Major histocompatibility locus
- Nonhuman primate
- Reactive arthritis
- Spondyloarthropathy
ASJC Scopus subject areas
- Immunology
- Genetics