AI Chat Paper
Note: Please note that the following content is generated by AMiner AI. SciOpen does not take any responsibility related to this content.
{{lang === 'zh_CN' ? '文章概述' : 'Summary'}}
{{lang === 'en_US' ? '中' : 'Eng'}}
Chat more with AI
PDF (9 MB)
Collect
Submit Manuscript AI Chat Paper
Show Outline
Outline
Show full outline
Hide outline
Outline
Show full outline
Hide outline
Review Article | Publishing Language: Chinese | Open Access

Research progress on the role of immune cells in the tumor microenvironment in the development and progression of oral squamous cell carcinoma

Xinyue LIAO1,2,3Yan FENG1,2,3Li YU2,3,4( )
Department of Pediatric Dentistry, The Affiliated Stomatology Hospital, Southwest Medical University, Luzhou 646000, China
School of Stomatology, Southwest Medical University, Luzhou 646000, China
Luzhou Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Southwest Medical University, Luzhou 646000, China
Department of Periodontal Mucosal Disease, The Affiliated Stomatology Hospital, Southwest Medical University, Luzhou 646000, China
Show Author Information

Abstract

Oral squamous cell carcinoma (OSCC), the most common type of head and neck malignancy, has a poor prognosis owing to its high invasiveness and high rate of cervical lymph node metastasis. The tumor microenvironment (TME) is a complex microenvironment that is essential for tumor cell survival. Tumor-associated immune cell (TAIC), the main stromal cell of TME, regulates the proliferation, invasion, epithelial-mesenchymal transformation (EMT), and anti-tumor immunity of OSCC. M2-tumor-associated macrophages (TAMs) promote the invasion and metastasis of OSCC through the macrophage migration inhibitory factor/NOD-like receptor family pyrin domain containing 3/interleukin (IL)-1β axis, while N2-tumor-associated neutrophils (TANs) regulate the proliferation and EMT of OSCC through the Janus kinase 2/signal transducer and activator of transcription 3 pathway. Meanwhile, myeloid-derived suppressor cells (MDSCs) accelerate the progression of OSCC by secreting IL-6, IL-10, and transforming growth factor (TGF)-β; T cells promote inflammation by secreting IL-17 and inhibit inflammation-mediated tumor immune response by secreting IL-10 and TGF-β; and natural killer (NK) cells recognize and attack OSCC cells to inhibit OSCC progression. TAIC interaction network also regulates OSCC progression. M2-TAMs regulate the invasion and metastasis of OSCC by promoting T cell apoptosis through the secretion of IL-10 and programmed death-ligand (PD-L) -1, while N2-TANs inhibit T cell proliferation and cytotoxicity by secreting LOX-1 and arginase-1. MDSCs inhibit the proliferation and anti-tumor effects of CD8+ T cells through the inactivation of programmed cell death (PD)-1/PD-L1 signaling. Additionally, MDSCs inhibit the proliferation of T cells by decreasing the expression of the CD3-zeta chain and interferon-γ (IFN-γ). Moreover, tumor-infiltrating lymphocytes and NK cells were found to be positively correlated in OSCC progression. Therefore, target regulation, related signaling pathways, and the interaction network of TAIC may serve as promising therapeutic targets in the immunotherapy of OSCC. In this review, we summarize the recent research on the effects of TAIC and their interaction network in the TME in the progression of OSCC and explore its application in the early diagnosis and treatment of OSCC.

CLC number: R78 Document code: A Article ID: 2096-1456(2025)02-0160-09

References

【1】
【1】
 
 
Journal of Prevention and Treatment for Stomatological Diseases
Pages 160-168

{{item.num}}

Comments on this article

Go to comment

< Back to all reports

Review Status: {{reviewData.commendedNum}} Commended , {{reviewData.revisionRequiredNum}} Revision Required , {{reviewData.notCommendedNum}} Not Commended Under Peer Review

Review Comment

Close
Close
Cite this article:
LIAO X, FENG Y, YU L. Research progress on the role of immune cells in the tumor microenvironment in the development and progression of oral squamous cell carcinoma. Journal of Prevention and Treatment for Stomatological Diseases, 2025, 33(2): 160-168. https://doi.org/10.12016/j.issn.2096-1456.202440045

1220

Views

14

Downloads

0

Crossref

1

Scopus

Received: 26 January 2024
Revised: 04 May 2024
Published: 20 February 2025
© 2025 by Editorial Department of Journal of Prevention and Treatment for Stomatological Diseases