Complement receptor 1 red cell expression is not controlled by the In(Lu) gene.
Complement receptor 1 red cell expression is not controlled by the In(Lu) gene.
复制标题
补体受体 1 红细胞表达不受 In(Lu) 基因控制。
DOI：
10.1046/j.1537-2995.1999.39070751.x
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发表时间：
1999
期刊：
影响因子：
2.9
通讯作者：
Shah,C
中科院分区：
文献类型：
--
作者：
Moulds,JM;Shah,C
背景：据报道，In(Lu)基因可抑制几种不属于路德教系统的血型抗原，包括诺普斯血型系统的高发生率抗原。由于已知携带 Knops 系统抗原的补体受体 1 (CR1) 具有红细胞 (RBC) 表达多态性，因此重新研究了 In(Lu) 在 Knops 系统抗原表达中的作用。 研究设计和方法：从具有 Lu(a–b–) 表型的 9 名供体中获取血液样本，并立即对 Lub、Kna、McCa、Sla 和 Sla 进行表型分析。是的。还对样本进行了 Lua、P1 和 AnWj 测试。通过免疫印迹研究这些供体的 CR1 和路德糖蛋白。使用酶联免疫吸附测定对 CR1 的红细胞表达进行定量，并通过 Southern blot 确定 CR1 高表达 (H) 或低表达 (L) 等位基因的遗传遗传。 结果：仅通过所有九个样品的吸收和洗脱技术即可证明 Lub；然而，高发生率的 Knops 系统抗原很容易通过血凝法检测到。两名 Lu(a–b–) 供体 (sibs) 在免疫印迹上显示出 78 和 85 kDa 的弱路德糖蛋白条带，而其他 7 个 Lu(a–b–) 样本则没有可检测到的糖蛋白。所有供体均具有 CR1*1，一名供体在免疫印迹上也具有 CR1*2。只有一名供者为 Lallele 纯合子，且所有的红细胞 CR1 拷贝数均在正常范围内。 结论：九名 Lu(a–b–) 表型供者表现出路德系统抗原的抑制，但 CR1 糖蛋白和 Knops 系统血型抗原的表达正常。这表明抑制路德系统抗原的基因不会抑制CR1或其相关血型抗原。
BACKGROUND:TheIn(Lu)gene reportedly suppresses several blood group antigens that are not part of the Lutheran system, including the high‐incidence antigens of the Knops blood group system. Because complement receptor 1 (CR1), which is known to carry the Knops system antigens, has a red cell (RBC) expression polymorphism, the role ofIn(Lu)in the expression of the Knops system antigens was reinvestigated.STUDY DESIGN AND METHODS:Blood samples from nine donors having the Lu(a–b–) phenotype were obtained and immediately phenotyped for Lub, Kna, McCa, Sla, and Yka. The samples were also tested for Lua, P1, and AnWj. Immunoblots were performed to study both the CR1 and Lutheran glycoproteins from these donors. RBC expression of CR1 was quantified with an enzyme‐linked immunosorbent assay, and the genetic inheritance of the high‐expression (H) or low‐expression (L) allele for CR1 was determined by Southern blot.RESULTS:Lubwas demonstrable only by absorption and elution techniques on all nine samples; however, the high‐incidence Knops system antigens were readily detectable by hemagglutination. Two Lu(a–b–) donors (sibs) demonstrated weak Lutheran glycoprotein bands of 78 and 85 kDa on immunoblots, while the other seven Lu(a–b–) samples had no detectable glycoprotein. All donors hadCR1*1, and one donor also hadCR1*2on immunoblot. Only one donor was homozygous for theLallele, and all had RBC copy numbers of CR1 within the normal range.CONCLUSIONS:Nine donors with the Lu(a–b–) phenotype showed suppression of the Lutheran system antigens but normal expression of CR1 glycoprotein and the Knops system blood group antigens. This suggests that the genes that suppress Lutheran system antigens do not suppress CR1 or its related blood group antigens.