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从 MTA1 鉴定的 HLA-A2 限制性表位可诱导抗原特异性细胞毒性 T 淋巴细胞反应。

HLA-A2-Restricted Epitopes Identified from MTA1 Could Elicit Antigen-Specific Cytotoxic T Lymphocyte Response.

机构信息

School of Life Sciences, Zhengzhou University, Zhengzhou 450001, China.

出版信息

J Immunol Res. 2018 Nov 25;2018:2942679. doi: 10.1155/2018/2942679. eCollection 2018.

DOI:10.1155/2018/2942679
PMID:30596107
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6286779/
Abstract

Overexpression of metastasis-associated protein 1 (MTA1) has been observed in many human malignancies and is significantly related to tumor invasion and metastasis, therapeutic resistance to radiation and chemotherapy, making MTA1 an ideal candidate tumor antigen. We identified several human leukocyte antigen- (HLA-) A2-restricted epitopes in MTA1 and evaluated their binding ability to HLA-A0201 molecules. Subsequently, a recombinant fragment encompassing the dominant epitopes, MTA1, was expressed, and the abilities of the selected epitopes of MTA1 and the MTA1 fragment to induce cytotoxic T lymphocytes (CTLs) were examined. Our results indicated that the epitopes and MTA1 fragment elicited HLA-A2-restricted and antigen-specific CTL responses both and . The new epitopes identified here may help promote the development of new therapeutic vaccines for HLA-A2 patients expressing MTA1.

摘要

过表达转移相关蛋白 1(MTA1)已在许多人类恶性肿瘤中观察到,并且与肿瘤侵袭和转移显著相关,对放疗和化疗的治疗耐药,使 MTA1 成为理想的候选肿瘤抗原。我们在 MTA1 中鉴定了几个人类白细胞抗原(HLA)-A2 限制性表位,并评估了它们与 HLA-A0201 分子的结合能力。随后,表达了包含主要表位的重组片段 MTA1,并检查了所选 MTA1 表位和 MTA1 片段诱导细胞毒性 T 淋巴细胞(CTL)的能力。我们的结果表明,表位和 MTA1 片段均能诱导 HLA-A2 限制性和抗原特异性 CTL 反应。这里鉴定的新表位可能有助于促进针对表达 MTA1 的 HLA-A2 患者的新型治疗性疫苗的开发。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ab/6286779/1e0f8e3c0ac3/JIR2018-2942679.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ab/6286779/8e1de2a532d3/JIR2018-2942679.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ab/6286779/8be38af254f5/JIR2018-2942679.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ab/6286779/eb2b765c7757/JIR2018-2942679.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ab/6286779/40f9742c3088/JIR2018-2942679.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ab/6286779/1e0f8e3c0ac3/JIR2018-2942679.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ab/6286779/8e1de2a532d3/JIR2018-2942679.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ab/6286779/8be38af254f5/JIR2018-2942679.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ab/6286779/eb2b765c7757/JIR2018-2942679.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ab/6286779/40f9742c3088/JIR2018-2942679.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ab/6286779/1e0f8e3c0ac3/JIR2018-2942679.005.jpg

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