Experimental spondyloarthropathy in HLA-B27 transgenic rats.

Rats of the LEW, F344, and PVG strains bearing high copy numbers of transgenes for HLA-B27 and human beta 2-microglobulin develop a multisystem disorder, many features of which resemble aspects of the human spondyloarthropathies, most dramatically axial and peripheral arthropathy. The disease is not seen in rats with comparable expression of HLA-B7, and so is relatively specific for HLA-B27. It requires T cells and another bone marrow derived cell, as well as an intact gut flora. Characteristic cytokine profiles distinguish the inflammatory infiltrates in the gut and the joint, and the earliest T cell infiltrates at these sites are polyclonal. Polymorphism at the Tap-2 peptide transporter locus has no significant effect on disease, whereas the DA strain background abrogates disease. The molecular role of the B27 molecule in disease remains to be elucidated, but there is good reason to believe that it will eventually yield to continued investigation of this animal model.