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. Author manuscript; available in PMC: 2019 Jun 27.
Published in final edited form as: Nat Rev Rheumatol. 2018 Dec;14(12):704–713. doi: 10.1038/s41584-018-0097-2
Higher B27 expression than other tissue sites?
Unique mechanical stressors/connective tissue (e.g. entheses, lens/ciliary body)?
More prone to dysregulation of homeostatic pathways (ER stress, autophagy, Treg, etc..)?
More susceptible to deposition of MAMP/microbes?
More permissive to infection due to immune privileged location?
Tissue tropism of infectious agents?
Mucosal-like addressins make them more susceptible to infiltration by gut-derived immune cells?
Increased expression of vascular adhesion molecules that promote infiltration of inflammatory immune cells (these may or may not be gut derived).
NOTE these properties may be acting in concert with other factors (e.g. viral infection or other stress of target tissue)