Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Apr 28;14:71. doi: 10.1186/s13045-021-01081-7

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

PMC Copyright notice

Fig. 8 — Novel HLA-A2.1-restricted ECM1-derived CTL epitope LA induces a significant DC-CTL and DC-NK antitumour effect. ① Identified novel HLA-A2.1 restricted ECM1-derived CTL epitope LA; ② LA was internalized into DCs mainly through phagocytosis; ③ LA facilitated DC maturation; ④ LA was presented on the surface of DCs via the vacuolar pathway; ⑤ LA passing the phagosome-to-cytosol pathway of DCs was degraded without exerting DC-CTL activation; ⑥ The LA/HLA-A2.1 complex was recognized by the TCR of CD8⁺ T cells. The phosphorylation level of ZAP70 was upregulated, inducing activation of CTL; ⑦ CTL could specifically kill tumour cells (DC-CTL interaction); ⑧ LA-activated TLR4 signal, then activated the p38 MAPK pathway to increase the expression of MICA/B on DCs; ⑨ Upregulated MICA/B expression activated NK cells via MICA/B-NKG2D signal; ⑩ LA enhanced NK antitumour effects (DC-NK crosstalk)