@article{286ea09b481e4b139a27f40c8951d95d,
title = "Spontaneous inflammatory disease in transgenic rats expressing HLA-B27 and human β2m: An animal model of HLA-B27-associated human disorders",
abstract = "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.",
author = "Hammer, {Robert E} and Maika, {Shanna D.} and Richardson, {James A} and Tang, {Jy Ping} and Taurog, {Joel D}",
note = "Funding Information: The technical contributions of Jana L. Hlavaty and Beverly Y. Hastings are gratefully acknowledged. The authors thank Dr. David T Armstrong for providing data prior to publication; Dr. Jonathan C. Howard for providing the pBS3.3/1 gene and data prior to publication; Dr. Jerry Y. Niederkorn and Marsha S. Pidherney for assistance with histologic sections of eyes; Dr. Albee Messing and Dr. Gerald A. Marks for assistance with preliminary characterization of the neurologic disturbance in the 21-4H line; and Dr. Joseph L. Goldstein, Dr. Michael S. Brown, and Dr. Peter E. Lipsky for helpful discussions and critical review of the manuscript. Ft. E. H. and J. D. T also wish to thank Dr. Lipsky for encouraging us to undertake this protect. This work was supported by NIH grants AR09989 (J. D. T and R. E. H.) and RR00890 (J. A. R.) and a grant from the North Texas Chapter of the Arthritis Foundation (J. D. T. and R. E. H.). J. D. T. was supported by NIH Research Career Development Award AR01756 during part of thll work.",
year = "1990",
month = nov,
day = "30",
doi = "10.1016/0092-8674(90)90512-D",
language = "English (US)",
volume = "63",
pages = "1099--1112",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",
number = "5",
}