Spontaneous inflammatory disease in transgenic rats expressing HLA-B27 and human β2m: An animal model of HLA-B27-associated human disorders

Robert E Hammer, Shanna D. Maika, James A Richardson, Jy Ping Tang, Joel D Taurog

Research output: Contribution to journalArticlepeer-review

778 Scopus citations


Humans who have inherited the human class I major histocompatibility allele HLA-B27 have a markedly increased risk of developing the multi-organ system diseases termed spondyloarthropathles. To investigate the role of B27 in these disorders, we introduced the B27 and human β2-microglobulin genes into rats, a species known to be quite susceptible to experimentally induced inflammatory disease. Rats from one transgenic line spontaneously developed inflammatory disease involving the gastrointestinal tract, peripheral and vertebral joints, male genital tract, skin, nails, and heart. This pattern of organ system involvement showed a striking resemblance to the B27-associated human disorders. These results establish that B27 plays a central role in the pathogenesis of the multi-organ system processes of the spondyloarthropathies. Elucidation of the role of B27 should be facilitated by this transgenic model.

Original languageEnglish (US)
Pages (from-to)1099-1112
Number of pages14
Issue number5
StatePublished - Nov 30 1990

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


Dive into the research topics of 'Spontaneous inflammatory disease in transgenic rats expressing HLA-B27 and human β<sub>2</sub>m: An animal model of HLA-B27-associated human disorders'. Together they form a unique fingerprint.

Cite this