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首页> 美国卫生研究院文献>Springer Open Choice >Potential link between MHC–self-peptide presentation and hematopoiesis; the analysis of HLA-DR expression in CD34-positive cells and self-peptide presentation repertoires of MHC molecules associated with paroxysmal nocturnal hemoglobinuria
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Potential link between MHC–self-peptide presentation and hematopoiesis; the analysis of HLA-DR expression in CD34-positive cells and self-peptide presentation repertoires of MHC molecules associated with paroxysmal nocturnal hemoglobinuria

机译：MHC-自肽呈递与造血作用之间的潜在联系；与阵发性夜间血红蛋白尿相关的MHC分子在CD34阳性细胞中的HLA-DR表达及自身肽呈递谱分析

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The mechanisms of MHC allele associations with paroxysmal nocturnal hemoglobinuria (PNH) and its aplastic anemia subtype (AA/PNH) remain unclear. It might be dependent on MHC molecule functional properties, such as a scope and frequency of antigen sampling and presentation. For documented PNH-associated MHC alleles we analyzed current reference databases on MHC molecule-eluted peptide presentation repertoires and searched for a range of presented peptides. MHC class II expression was measured on CD34+ cells and appeared to be increased in PNH patients. Two class I alleles (HLA-A*24:02 and B*18:01) have been previously confirmed to associate with protection and increased risk of AA/PNH, respectively. Their product molecules presented immunodominant epitopes derived from proapoptotic (serine/threonine–protein phosphatase) and antiapoptotic (phospholipase D), respectively, intracellular enzymes dependent on phosphoinositide (PI) content. For total PNH and non-aplastic PNH (n/PNH) subtype-associated DRB1*15:01 and DRB1*04:01 class II molecules presentation of exceptionally broad arrays of their own peptide fragments has been found. We conclude that self antigen peptides presented with high frequency in the context of MHC molecules of increased expression may be involved in the immune recognition and the regulation of HSC in the periphery. The block in the normal plasma membrane PI production due to the PIG-A mutation can help explain the differences in the activation of intracellular regulatory pathways observed between PNH and normal HSC. This is evident in the variation in MHC association patterns and peptide presentation repertoires between these two groups of patients.Electronic supplementary materialThe online version of this article (doi:10.1007/s12013-012-9435-1) contains supplementary material, which is available to authorized users.
机译：MHC等位基因与阵发性夜间血红蛋白尿（PNH）及其再生障碍性贫血亚型（AA / PNH）的机制尚不清楚。它可能取决于MHC分子的功能特性，例如抗原采样和呈递的范围和频率。对于已记录的PNH相关MHC等位基因，我们分析了MHC分子洗脱的肽呈递谱库中的当前参考数据库，并搜索了一系列呈递的肽。在CD34 +细胞上测量了II类MHC表达，并且在PNH患者中似乎有所增加。先前已确认两个I类等位基因（HLA-A * 24：02和B * 18：01）分别与保护作用和AA / PNH风险增加相关。他们的产物分子呈现出分别来自促细胞凋亡（丝氨酸/苏氨酸-蛋白磷酸酶）和抗凋亡（磷脂酶D）的免疫优势表位，细胞内酶取决于磷酸肌醇（PI）的含量。对于总的PNH和非再生性PNH（n / PNH），与亚型相关的DRB1 * 15：01和DRB1 * 04：01 II类分子已发现其自身肽片段的排列异常广泛。我们得出的结论是，在表达增加的MHC分子中以高频率出现的自身抗原肽可能参与免疫识别和外周血HSC的调节。 PIG-A突变导致正常质膜PI生成受阻，可以帮助解释在PNH和正常HSC之间观察到的细胞内调节途径激活的差异。这在这两组患者之间的MHC关联模式和肽呈递方式的差异中就很明显。电子补充材料本文的在线版本（doi：10.1007 / s12013-012-9435-1）包含补充材料，可用于授权用户。

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