Abstract
Transgenic (Tg) rats carrying high copy numbers of both B27 and human β2m on either the Lewis or F344 genetic backgrounds spontaneously develop a multisystem inflammatory disease similar to human SpA with arthritis, gut and male GU inflammation and psoriasiform skin and nail changes1. Histological examination of the lesions suggested a disease with an immunological basis1. Cell transfer experiments2 and the derivation of germ free animals3 suggest a critical role for antigen presenting cells (APC), T cells and the gut flora in the joint and gut inflammation.
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