PMID- 37944422
OWN - NLM
STAT- MEDLINE
DCOM- 20231127
LR  - 20231127
IS  - 1568-7856 (Electronic)
IS  - 1568-7856 (Linking)
VI  - 132
DP  - 2023 Dec
TI  - Regulation of DNA damage-induced HLA class I presentation.
PG  - 103590
LID - S1568-7864(23)00144-1 [pii]
LID - 10.1016/j.dnarep.2023.103590 [doi]
AB  - Immune checkpoint inhibitors (ICI) are cancer therapies that restore anti-tumor 
      immunity; however, only a small percentage of patients have been completely cured 
      by ICI alone. Multiple approaches in combination with other modalities have been 
      used to improve the efficacy of ICI therapy. Among conventional cancer 
      treatments, radiotherapy or DNA damage-based chemotherapy is a promising 
      candidate as a partner of ICI because DNA damage signaling potentially stimulates 
      immune activities turning the tumor's immune environment into hot tumors. 
      Programmed death-ligand 1 (PD-L1) and human leukocyte antigen class I (HLA-I), 
      which are immune ligands, regulate the balance of anti-tumor immunity in the 
      tumor microenvironment. PD-L1 functions as a brake to suppress cytotoxic T cell 
      activity, whereas HLA-I is an immune accelerator that promotes the downstream of 
      the T cell signaling. Accumulating evidence has demonstrated that DNA damage 
      enhances the presentation of HLA-I on the surface of damaged cells. However, it 
      is unclear how signal transduction in DNA-damaged cells upregulates the 
      presentation of HLA-I with antigens. Our recent study uncovered the mechanism 
      underlying DNA damage-induced HLA-I presentation, which requires polypeptide 
      synthesis through a pioneer round of translation. In this review, we summarize 
      the latest overview of how DNA damage stimulates antigen production presented by 
      HLA-I.
CI  - Copyright (c) 2023 Elsevier B.V. All rights reserved.
FAU - Uchihara, Yuki
AU  - Uchihara Y
AD  - Division of Molecular Oncological Pharmacy, Faculty of Pharmacy, Keio University, 
      Tokyo, Japan.
FAU - Shibata, Atsushi
AU  - Shibata A
AD  - Division of Molecular Oncological Pharmacy, Faculty of Pharmacy, Keio University, 
      Tokyo, Japan. Electronic address: shibata.at@keio.jp.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20231101
PL  - Netherlands
TA  - DNA Repair (Amst)
JT  - DNA repair
JID - 101139138
RN  - 0 (B7-H1 Antigen)
RN  - 0 (Histocompatibility Antigens Class I)
SB  - IM
MH  - Humans
MH  - *B7-H1 Antigen/metabolism
MH  - Histocompatibility Antigens Class I/genetics/metabolism
MH  - *Neoplasms/drug therapy/genetics
MH  - DNA Damage
MH  - T-Lymphocytes/metabolism
MH  - Tumor Microenvironment
OTO - NOTNLM
OT  - DNA damage
OT  - DNA damage-induced HLA (di-HLA) presentation
OT  - HLA class I
OT  - Immune response
OT  - Pioneer round of translation
COIS- Declaration of Competing Interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/11/10 00:44
MHDA- 2023/11/27 12:42
CRDT- 2023/11/09 18:14
PHST- 2023/06/28 00:00 [received]
PHST- 2023/10/02 00:00 [revised]
PHST- 2023/10/17 00:00 [accepted]
PHST- 2023/11/27 12:42 [medline]
PHST- 2023/11/10 00:44 [pubmed]
PHST- 2023/11/09 18:14 [entrez]
AID - S1568-7864(23)00144-1 [pii]
AID - 10.1016/j.dnarep.2023.103590 [doi]
PST - ppublish
SO  - DNA Repair (Amst). 2023 Dec;132:103590. doi: 10.1016/j.dnarep.2023.103590. Epub 
      2023 Nov 1.