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HLA I 类分子与伴有核仁磷酸蛋白基因突变的急性髓系白血病患者的患病率和结局的相关性研究。

Association of HLA class I type with prevalence and outcome of patients with acute myeloid leukemia and mutated nucleophosmin.

机构信息

Department of Proteomics, Institute of Hematology and Blood Transfusion, Prague, Czech Republic.

Department of Internal Medicine I, University Hospital Carl Gustav Carus, Dresden, Germany.

出版信息

PLoS One. 2018 Dec 17;13(12):e0204290. doi: 10.1371/journal.pone.0204290. eCollection 2018.

DOI:10.1371/journal.pone.0204290
PMID:30557403
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6296532/
Abstract

Acute myeloid leukemia with mutated nucleophosmin (NPMc+ AML) forms a distinct AML subgroup with better prognosis which can potentially be associated with immune response against the mutated nucleophosmin (NPM). As the T-cell-mediated immunity involves antigen presentation on HLA class I molecules, we hypothesized that individuals with suitable HLA type could be less prone to develop NPMc+ AML. We compared HLA class I distribution in NPMc+ AML patient cohort (398 patients from 5 centers) with the HLA allele frequencies of the healthy population and found HLA-A02, B07, B40 and C07 underrepresented in the NPMc+ AML group. Presence of B07 or C07:01 antigen was associated with better survival in patients without concomitant FLT3 internal tandem duplication. Candidate NPM-derived immunopeptides were found for B40 and B07 using prediction software tools. Our findings suggest that a T-cell-mediated immune response could actually explain better prognosis of NPMc+ patients and provide a rationale for attempts to explore the importance of immunosuppressive mechanisms in this AML subgroup.

摘要

伴核磷蛋白 N 端突变的急性髓系白血病（NPMc+ AML）是一种具有较好预后的 AML 亚组，其可能与针对突变核磷蛋白（NPM）的免疫反应有关。由于 T 细胞介导的免疫涉及 HLA I 类分子上的抗原呈递，我们假设具有合适 HLA 类型的个体不太可能发展为 NPMc+ AML。我们比较了 NPMc+ AML 患者队列（来自 5 个中心的 398 例患者）与健康人群的 HLA 等位基因频率，发现 NPMc+ AML 组中 HLA-A02、B07、B40 和 C07 表达不足。在没有同时伴有 FLT3 内部串联重复的患者中，存在 B07 或 C07:01 抗原与更好的生存相关。使用预测软件工具，发现了针对 B40 和 B07 的候选 NPM 衍生免疫肽。我们的研究结果表明，T 细胞介导的免疫反应实际上可以解释 NPMc+患者预后较好的原因，并为探索免疫抑制机制在该 AML 亚组中的重要性提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7ff/6296532/cae29dc9f8dd/pone.0204290.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7ff/6296532/a497f356c274/pone.0204290.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7ff/6296532/f4b3d6a3a4d3/pone.0204290.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7ff/6296532/cae29dc9f8dd/pone.0204290.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7ff/6296532/a497f356c274/pone.0204290.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7ff/6296532/f4b3d6a3a4d3/pone.0204290.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7ff/6296532/cae29dc9f8dd/pone.0204290.g003.jpg

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