The Loll et al research fits with the idea that the flexibility and unfolding and tendency to dimerize may be important to how HLA-B27 causes disease. Additionally, the results indicate that more research is needed to understand the implications of that to the cells that express HLA-B27, Dr. Colbert says.
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“The biggest implication for therapy would be to understand how HLA-B27 contributes to this disease. In other words, can we prevent HLA-B27 from dimerizing? Can we fix a subtype associated with disease, cause it to fold better and not dimerize?” That is not yet a possibility, but researchers continue to investigate HLA-B27 and its aberrant features at several labs around the world.
Kathy L. Holliman, MEd, is a medical writer based in Beverly, Mass.
- Loll B, Fabian H, Huser H, et al. Increased conformational flexibility of HLA-B*27 subtypes associated with ankylosing spondylitis. Arthritis Rheumatol. 2016 May;68(5):1172–1182.
- Powis SJ, Colbert RA. Editorial: HLA-B27: The story continues to unfold. Arthritis Rheumatol. 2016 May;68(5):1057–1059.
- Bowness P. HLA-B27. Annu Rev Immunol. 2015;33:29–48.