| Autor: |
Weinreich, S. S., Hoebe-Hewryk, Bogda, van der Horst, A. R., Boog, Claire J. P., Ivanyi, Pavol |
| Zdroj: |
Immunogenetics; May1997, Vol. 46 Issue 1, p35-40, 6p |
| Abstrakt: |
Ankylosing enthesopathy (ANKENT) is a spontaneous mouse joint disease with strikingly similar pathology to human HLA-B27-associated enthesopathies such as ankylosing spondylitis. In C57Bl/10 mice, transgenic HLA-B*2702 as well as H2 genes have been shown to be relative risk factors for ANKENT. To investigate the role of major histocompatibility complex (MHC) class I expression in disease pathogenesis, ANKENT occurrence was compared among β2-microglobulin (β2m) knockout littermates with or without transgenes for HLA-B*2702 and human β2m. In the knockout phenotype lacking β2m, ANKENT occurrence is significantly reduced ( P = 0.016). In the absence of β2m, B*2702 is not detected on the cell membrane, nor does it increase the risk for ANKENT. This means that the previous finding that HLA-B*2702 increases susceptibility to ANKENT in C57Bl/10 mice cannot be ascribed to a transgene insertion effect. Rather, in order to increase disease susceptibility, B*2702 must be coexpressed with mouse β2m (mo-β2m). In contrast, when HLA-B*2702 is expressed with β2m of human origin, disease susceptibility is not affected. Thus, both H2b-derived class I heterodimers and HLA-B*2702/mo-β2m heterodimers contribute to ANKENT susceptibility. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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