Ochs H D, Rosenfeld S I, Thomas E D, Giblett E R, Alper C A, Dupont B, Schaller J G, Gilliland B C, Hansen J A, Wedgwood R J
N Engl J Med. 1977 Mar 3;296(9):470-5. doi: 10.1056/NEJM197703032960902.
In an attempt to map the gene (or genes) controlling the synthesis fo the fourth component of complement (C4), we performed linkage studies in a family with hereditary C4 deficiency. The proband, a seven-year-old boy with lupus erythematosus, consistently lacked deteftable serum C4 by both functional and protein measurements. The complement defect was transmitted as an autosomal recessive disorder. Eight of 15 family members were considered to be heterozygotes, seven because of low C4 levels and one because of genetic data (obligate heterozygote). The gene (or genes) coding for C4 deficiency appeared to be linked to the major histocompatibility complex (A2,B12,DW2 on the maternal side and A2,BW15,LD108 on the paternal side) and to other markers known to be in close proximity to the histocompatibility complex on chromosome 6 (phosphoglucomutase-3, glyoxalase-1 and properdin factor B).
为了定位控制补体第四成分(C4)合成的一个或多个基因,我们在一个遗传性C4缺乏的家族中进行了连锁研究。先证者是一名患有红斑狼疮的7岁男孩,通过功能和蛋白质检测均始终未能检测到血清C4。补体缺陷作为常染色体隐性疾病遗传。15名家族成员中有8人被认为是杂合子,7人是因为C4水平低,1人是基于遗传数据(肯定杂合子)。编码C4缺乏的一个或多个基因似乎与主要组织相容性复合体连锁(母方为A2、B12、DW2,父方为A2、BW15、LD108),也与已知在6号染色体上与组织相容性复合体紧密相邻的其他标记连锁(磷酸葡萄糖变位酶-3、乙二醛酶-1和备解素因子B)。