PMID- 18290741
OWN - NLM
STAT- MEDLINE
DCOM- 20080410
LR  - 20080222
IS  - 1092-0684 (Electronic)
IS  - 1092-0684 (Linking)
VI  - 24
IP  - 1
DP  - 2008
TI  - The pathogenesis of ankylosing spondylitis.
PG  - E3
LID - 10.3171/FOC/2008/24/1/E3 [doi]
AB  - Ankylosing spondylitis (AS) is a chronic inflammatory disease that can cause 
      significant functional complications by affecting the sacroiliac joints and axial 
      skeleton. Despite a longstanding knowledge about the familial associations of 
      this disease, particularly among patients positive for human leukocyte antigen 
      (HLA)-B27, the fundamental pathogenetic mechanism by which this disease arises in 
      genetically susceptible individuals remains ill defined. Furthermore, the 
      molecular predilection for characteristic articular site involvement remains 
      under ongoing investigation. Current theories about the HLA-B27 association range 
      from the presentation of novel arthritogenic peptides, to abnormal autoimmune 
      stimulation, to anomalous microbial tolerance. The immune effectors of this 
      damage include CD4+, CD8+, and natural killer cells, with marked heterogeneity at 
      different sites. Biomechanical stresses may trigger this disease by exposing the 
      body to previously immune-sequestered autoantigens or by providing a route for 
      bacterial seeding. Environmental triggers such as infection have not been 
      definitively established but may represent a primary pathogenic step in a 
      molecular-mimicry process. In this article, the authors review the current 
      literature on the origin and pathophysiology of AS, focusing on genetic and 
      molecular associations, consequent pathomechanisms, and associated triggers. An 
      improved understanding of the sequence of molecular events that predispose and 
      initiate the onset of this disease will allow for more specific and targeted 
      therapy and better avoidance of the significant side effects of systemic 
      immunomodulation.
FAU - Shamji, Mohammed F
AU  - Shamji MF
AD  - Division of Neurosurgery, The Ottawa Hospital and University of Ottawa, Canada.
FAU - Bafaquh, Mohammed
AU  - Bafaquh M
FAU - Tsai, Eve
AU  - Tsai E
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Neurosurg Focus
JT  - Neurosurgical focus
JID - 100896471
RN  - 0 (HLA-B27 Antigen)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
SB  - IM
MH  - HLA-B27 Antigen/*physiology
MH  - Humans
MH  - Intercellular Signaling Peptides and Proteins/physiology
MH  - Klebsiella/immunology
MH  - Spondylitis, Ankylosing/*etiology/pathology/*physiopathology
RF  - 118
EDAT- 2008/02/23 09:00
MHDA- 2008/04/11 09:00
CRDT- 2008/02/23 09:00
PHST- 2008/02/23 09:00 [pubmed]
PHST- 2008/04/11 09:00 [medline]
PHST- 2008/02/23 09:00 [entrez]
AID - 10.3171/FOC/2008/24/1/E3 [doi]
PST - ppublish
SO  - Neurosurg Focus. 2008;24(1):E3. doi: 10.3171/FOC/2008/24/1/E3.