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A signal peptide derived from Hsp60 induces protective cytotoxic T lymphocyte immunity against lymphoid malignancies independently of TAP and classical MHC-I.

Authors
  • Chen, Xun-Rui1
  • Yuan, Hai-Hua1
  • Guo, Jia-Hui1
  • Zhang, Wen-Ying1
  • Li, Qian-Qian1
  • Huang, Guo-Ding2
  • Zhang, Yan-Jie3
  • Jiang, Bin4
  • Liu, Feng5
  • 1 Oncology Department, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 201900, China. , (China)
  • 2 Oncology Department, Hainan Western Central Hospital, Danzhou, 571700, Hainan Province, China. , (China)
  • 3 Oncology Department, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 201900, China. Electronic address: [email protected] , (China)
  • 4 Oncology Department, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 201900, China. Electronic address: [email protected] , (China)
  • 5 Oncology Department, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 201900, China; Oncology Department, Hainan Western Central Hospital, Danzhou, 571700, Hainan Province, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Cancer letters
Publication Date
Aug 20, 2020
Volume
494
Pages
47–57
Identifiers
DOI: 10.1016/j.canlet.2020.08.016
PMID: 32829008
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Hsp60sp, a signal peptide derived from the leader sequence of heat shock protein 60 kDa (Hsp60), is a Qa-1/HLA-E-binding peptide. We previously showed that Hsp60sp-specific CD8+ T cells are involved in the immunoregulation of autoimmune diseases by controlling the response of self-reactive lymphocytes. Here, we report that Hsp60sp-specific CD8+ T cells killed malignant lymphocytes in vitro independently of transporter associated with antigen processing (TAP) and classical MHC-I expression. Induction of this cytotoxic T lymphocyte (CTL) response in vivo, either by adoptive transfer of in vitro-amplified CTLs or peptide-loaded dendritic cell immunization, resulted in effective control of lymphoid tumors, including TAP- or classical MHC-I-deficient cells. Hsp60sp-specific immune activation combined with programmed cell death protein 1 (PD-1) blocking synergistically restrained mouse lymphoma development. Importantly, Hsp60sp-specific CD8+ T cells did not negatively affect normal tissues and cells. Our data suggest that Hsp60sp-based immunotherapy is an inviting strategy to control lymphoid malignancies. Copyright © 2020 Elsevier B.V. All rights reserved.

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