Innate immune response restarts adaptive immune response in tumors

Wen-Shan Li; Qing-Qing Zhang; Qiao Li; Shang-Yu Liu; Guo-Qiang Yuan; Ya-Wen Pan

doi:10.3389/fimmu.2023.1260705

Innate immune response restarts adaptive immune response in tumors

Front Immunol. 2023 Sep 14:14:1260705. doi: 10.3389/fimmu.2023.1260705. eCollection 2023.

Authors

Wen-Shan Li^{1

2

3}, Qing-Qing Zhang⁴, Qiao Li^{1

2}, Shang-Yu Liu^{1

2}, Guo-Qiang Yuan^{1

2}, Ya-Wen Pan^{1

2}

Affiliations

¹ The Department of Neurosurgery, The Second Hospital of Lanzhou University, Lanzhou, Gansu, China.
² Key Laboratory of Neurology of Gansu Province, The Second Hospital of Lanzhou University, Lanzhou, Gansu, China.
³ Department of Neurosurgery, Qinghai Provincial People's Hospital, Xining, Qinghai, China.
⁴ Department of Respiratory and Critical Care Medicine, Qinghai University Affiliated Hospital, Xining, Qinghai, China.

Abstract

The imbalance of immune response plays a crucial role in the development of diseases, including glioblastoma. It is essential to comprehend how the innate immune system detects tumors and pathogens. Endosomal and cytoplasmic sensors can identify diverse cancer cell antigens, triggering the production of type I interferon and pro-inflammatory cytokines. This, in turn, stimulates interferon stimulating genes, enhancing the presentation of cancer antigens, and promoting T cell recognition and destruction of cancer cells. While RNA and DNA sensing of tumors and pathogens typically involve different receptors and adapters, their interaction can activate adaptive immune response mechanisms. This review highlights the similarity in RNA and DNA sensing mechanisms in the innate immunity of both tumors and pathogens. The aim is to enhance the anti-tumor innate immune response, identify regions of the tumor that are not responsive to treatment, and explore new targets to improve the response to conventional tumor therapy and immunotherapy.

Keywords: DNA sensing; RNA sensing; crosstalk; glioblastoma; type I interferon.

Publication types

Review
Research Support, Non-U.S. Gov't

MeSH terms

Adaptive Immunity
DNA
Humans
Immunity, Innate / physiology
Interferon Type I*
Neoplasms*
RNA
Signal Transduction

Substances

DNA
Interferon Type I
RNA

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by grants from the National Natural Science Foundation of China (81960541/82060455).