Spontaneous inflammatory disease in HLA-B27 transgenic mice does not require transporter of antigenic peptides |
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Authors: | Khare S D Lee S Bull M J Hanson J Luthra H S David C S |
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Institution: | Department of Immunology, Mayo Clinic and Medical School, Rochester, Minnesota, 55905, USA. |
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Abstract: | HLA-B27 is strongly linked with a group of human diseases called spondyloarthropathies. Even though HLA-B27 as an MHC class I molecule would be expected to present endogenously processed peptides such as cytosolic or viral proteins, many of the B27-linked diseases begin after an infection with an enterobacteria, an exogenous antigen. In our previous studies, we have described development of spontaneous inflammatory disease in HLA-B27 transgenic mice expressing beta(2)m free heavy chains on the cell surface. In order to address the role of endogenous versus exogenous antigens and a role for Tap genes in the development of spontaneous diseases, mice lacking Tap-1 (knockout) were mated to HLA-B27/human beta(2)m transgenic mice. B27(+)/human beta(2)m(+) double-transgenic mice (without mouse beta(2)m) lacking the Tap-1 gene developed spontaneous inflammatory disease similar to wild-type Tap-1 gene-expressing counterparts. Our data demonstrate that peptide transporters (Tap) were not involved in the development of spontaneous inflammatory disease in B27(+)/human beta(2)m transgenic animals. |
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Keywords: | HLA-B27 spondyloarthropathy reactive arthritis TAP polymorphism endogenous peptides |
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