HLA-A 和 HLA-DRB1 可能在卵巢畸胎瘤相关抗 N-甲基-D-天冬氨酸受体脑炎中发挥独特作用。
HLA-A and HLA-DRB1 may play a unique role in ovarian teratoma-associated anti-N-methyl-D-aspartate receptor encephalitis.
机构信息
Department of Obstetrics and Gynecology, International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiaotong University, No. 910, Hengshan Rd, Shanghai, 200030, China.
Department of Pathology, International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200030, China.
出版信息
Reprod Biol Endocrinol. 2020 Nov 7;18(1):107. doi: 10.1186/s12958-020-00661-5.
BACKGROUND
Ovarian teratoma-associated anti-N-methyl-D-aspartate receptor encephalitis (NMDAR-E) is a severe autoimmune neurological disorder, and the influence of teratoma-induced autoantibodies on the pathogenesis remains unclear.
METHODS
Ovarian teratoma tissues were collected from teratoma patients with and without NMDAR-E. Proteins were extracted and then analyzed using iTRAQ-coupled LC-MS/MS, which was followed by bioinformatics analysis. Candidate proteins were verified by Western blotting and immunohistochemistry.
RESULTS
In total, 36 differentially expressed proteins (DEPs) were identified between the control group and NMDAR-E group, and the bioinformatics analysis revealed that the DEPs were mainly involved in immune-related pathways, especially HLA-A and HLA-DRB1. The western blotting results for HLA-A and HLA-DRB1 were consistent with the results of the iTRAQ analysis. Additionally, the immunohistochemical data revealed that the aggregation of HLA-A (+) and HLA-DRB1 (+) cells was more apparent in the teratoma tissues of NMDAR-E patients compared with that in the tissues of controls.
CONCLUSION
Our investigation indicated that HLA-A and HLA-DRB1 might be involved in mediating ovarian teratoma-associated NMDAR-E. These findings provide new insights into the pathophysiological mechanisms and provide information for the functional exploration of proteins in the future.
背景
卵巢畸胎瘤相关抗 N-甲基-D-天冬氨酸受体脑炎（NMDAR-E）是一种严重的自身免疫性神经疾病，而畸胎瘤诱导的自身抗体对发病机制的影响尚不清楚。
方法
收集有和无 NMDAR-E 的畸胎瘤患者的畸胎瘤组织。提取蛋白质，然后使用 iTRAQ 耦联 LC-MS/MS 进行分析，接着进行生物信息学分析。通过 Western blot 和免疫组织化学验证候选蛋白。
结果
共鉴定出对照组和 NMDAR-E 组之间 36 个差异表达蛋白（DEPs），生物信息学分析表明 DEPs 主要涉及免疫相关途径，特别是 HLA-A 和 HLA-DRB1。HLA-A 和 HLA-DRB1 的 Western blot 结果与 iTRAQ 分析结果一致。此外，免疫组化数据显示，与对照组相比，NMDAR-E 患者的畸胎瘤组织中 HLA-A（+）和 HLA-DRB1（+）细胞的聚集更为明显。
结论
我们的研究表明，HLA-A 和 HLA-DRB1 可能参与介导卵巢畸胎瘤相关的 NMDAR-E。这些发现为病理生理机制提供了新的见解，并为未来蛋白质的功能探索提供了信息。
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