Several rodent models have been developed for studying the role of HLA-B27 in conferring susceptibility to rheumatic diseases. Mice and rats expressing HLA-B27 as a transgene develop arthritic symptoms, including swelling of peripheral joints and nail deformation, which vary according to species, the conditions in which the animal was raised, the copy number of the transgene, and the inclusion of additional genetic modifications. The HLA-B27 transgenic model was first established in rats, which develop spontaneous arthritic symptoms when expression of HLA-B27 is paired with expression of human p2-microglobulin (P2m) . Disease in this model is also dependent upon a high copy number of HLA-B27, and upon raising the animals in an environment that is not germ-free . Mice transgenic only for HLA-B27 do not develop disease. Spontaneous arthritis in HLA-B27 transgenic mice requires a deficiency in murine P2m and housing conditions that are not germ-free [55, 56] or the inclusion of human P2m as a second transgene . Removal from germ-free colonies is also essential to arthritis induction in the mice transgenic for both HLA-B27 and human P2m. The lack of requirement for P2m in these mice is interesting, since normal functions of MHC Class I require pairing with P2m prior to peptide binding and presentation of peptide by MHC Class I on the cell surface.
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