Ota M, Bahram S, Katsuyama Y, Saito S, Nose Y, Sada M, Ando H, Inoko H
Department of Legal Medicine, Shinshu University School of Medicine, Nagano, Japan.
Tissue Antigens. 2000 Sep;56(3):268-71. doi: 10.1034/j.1399-0039.2000.560309.x.
A 100-kb deletion including the MICA gene was recently reported in the HLA-B48 (B*4801)-associated haplotype in Japanese. Interestingly, this MICA deletion is accompanied by a MICB null allele, MICB0107N. In order to further investigate the universality of the apparent tight linkage between these two events, we present data on high-resolution deletion mapping of eight HLA-B48-homozygous individuals. Among these, five carried the MICA deletion linked to MICB0107N, as originally reported. Conversely, the remaining three possessed an intact MICA gene of MICA008 or MICA010 allelic variant associated this time with a putative expressed MICB allele, MICB0102. These results may imply that the expression of both MICA and MICB molecules is indispensable to viability through a yet-to-be understood mutual interaction in immune surveillance.
最近有报道称，在日本人群中，与HLA - B48（B*4801）相关的单倍型中存在一个包含MICA基因的100 kb缺失。有趣的是，这种MICA缺失伴随着一个MICB无效等位基因MICB0107N。为了进一步研究这两个事件之间明显紧密连锁的普遍性，我们展示了8名HLA - B48纯合个体的高分辨率缺失图谱数据。其中，有5名个体携带与MICB0107N连锁的MICA缺失，这与最初报道的情况一致。相反，其余3名个体拥有完整的MICA基因，为MICA008或MICA010等位基因变体，此次与一个推定的可表达MICB等位基因MICB0102相关。这些结果可能意味着，通过免疫监视中尚未明确的相互作用，MICA和MICB分子的表达对于生存能力而言都是不可或缺的。
