Abstract：
:The HLA-B27 molecule is strongly associated with the spondyloarthropathies, a group of chronic inflammatory diseases, affecting the skeleton, the bowel and the skin. This association has been largely studied, but mechanisms of pathology remain unclear. The HLA-B27 transgenic rats develop a spontaneous disease that strikingly resembles human spondyloarthropathies, dependent of bacterial flora and implicating the immune system. The presence of CD4+ T cells is required, and antigen presenting cells (APC) expressing high levels of HLA-B27 likely play an important role. Indeed, APC are defective in naive T lymphocytes stimulation. This default appears to implicate the APC/T cells contact, and may result in a loss of tolerance toward microbial flora. Two models of skeletal inflammation linked to HLA-B27 have been developed in mice. The ANKENT mice develop a spontaneous ossifying enthesitis affecting ankle and tarsal joints, with increased frequency in the presence of an HLA-B27 transgene. The HLA-B27 transgenic mice lacking endogenous beta2 microglobulin develop arthritis of hind-paws. In this model, homodimers of B27 heavy chains could be implicated in the pathogenesis by presenting exogenous peptides to CD4+ T cells.
journal_name
Joint Bone Spinejournal_title
Joint bone spineauthors
Hacquard-Bouder C,Ittah M,Breban Mdoi
10.1016/j.jbspin.2005.03.016subject
Has Abstractpub_date
2006-03-01 00:00:00pages
132-8issue
2eissn
1297-319Xissn
1778-7254pii
S1297-319X(05)00130-2journal_volume
73pub_type
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