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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Stagg, A.J., Breban, M., Hammer, R.E., Knight, S.C., Taurog, J.D. (1995). Defective Dendritic Cell (DC) Function in a HLA-B27 Transgenic Rat Model of Spondyloarthropathy (SpA). In: Banchereau, J., Schmitt, D. (eds) Dendritic Cells in Fundamental and Clinical Immunology. Advances in Experimental Medicine and Biology, vol 378. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1971-3_125
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DOI: https://doi.org/10.1007/978-1-4615-1971-3_125
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