Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster Display session

356P - DDR2 inhibition reveals a T cell immune checkpoint that controls lung cancer immunosurveillance

Date

28 Mar 2025

Session

Poster Display session

Presenters

Shuai ZHANG

Citation

Journal of Thoracic Oncology (2025) 20 (3): S208-S232. 10.1016/S1556-0864(25)00632-X

Authors

S. ZHANG1, Y. Jin2

Author affiliations

  • 1 HUST - Huazhong University of Science and Technology, Wuhan/CN
  • 2 Union Hospital, Tongji Medical College, Huazhong University of Science and Technology/ Cancer Center Union Hospital, 430074 - Wuhan/CN

Resources

Login to get immediate access to this content.

If you do not have an ESMO account, please create one for free.

Abstract 356P

Background

Immune checkpoint inhibitors have shown significant therapeutic responses against lung cancer. However, reinvigoration of antitumor immunity remains a big challenge.

Methods

We use flow cytometry to test the capacity of 640 tyrosine kinase inhibitors (TKIs) to increase the expression of CD69 and ICOS in CD8+T cells. In vitro and in vivo studies were further used to validate the T cell activation effect of screened TKIs. Crispr-cas9 knockout was used to identify the potential targets of screened TKIs.

Results

The screening of 640 tyrosine kinase inhibitors yielded two major hits, merestinib and WRG-28. Merestinib and WRG-28 caused a dose-dependent increase in the expression of CD69, ICOS, and the production of interferon-γ (IFN-γ) in mouse primary CD8+T cells. Merestinib and WRG-28 also decreased the expression of PD-1 and TIGIT (T cell immunoglobulin and ITIM domain) in activated mouse primary CD8+T cells. Mechanistically, merestinib and WRG-28 share the same target, DDR2 (discoidin domain receptor tyrosine kinase 2), knockout of DDR2 phenocopied these effects. Furthermore, merestinib and WRG-28 caused the rapid (10 min) activation of the T-cell receptorproximal signaling kinases, as detectable by immunoblot detection of activating phosphorylations affecting LAT (on tyrosine residue 220) and LCK (on tyrosine 394). Utilizing immunocompetent and immunodeficient mouse models, we further demonstrated that the merestinib or WRG-28 treatment suppressed the tumor growth of TC-1 lung cancer, leading to an improved prognosis through the restoration of cytotoxic T lymphocyte responses and reinstatement of anti-cancer immunosurveillance in vivo.

Conclusions

In conclusion, merestinib and WRG-28 restrain lung cancer immunosurveillance. DDR2 is a potential novel T-cell immune checkpoint.

Legal entity responsible for the study

Huazhong Univercity of Science and Technology, Wuhan, China.

Funding

National Natural Science Foundation of China (no. 82070099, no. 82330003 and no.82300124).

Disclosure

All authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.