Related Experiment Video
Updated: Jun 6, 2025

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
Published on: May 10, 2022
Hyperactivity of the IL-33-ILC2s-IL-13-M-MDSCs axis promotes cervical cancer progression
Bihui Wang1, Yuejie Zhu2, Yulian Zhang1
1Department of Gynecology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China; State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China.
Abstract:
The interleukin-33(IL-33) - group 2 innate lymphoid cells (ILC2s) - interleukin-13(IL-13) - monocytic myeloid-derived suppressor cells (M-MDSCs) axis plays a critical role in promoting immune evasion in tumors; however, its specific function in cervical cancer remains poorly understood. In this study, we observed that the proportion of IL-33-ILC2s-IL-13-M-MDSCs were significantly elevated in both cervical cancer patients and the subcutaneous U14 cervical cancer mouse model, compared to normal controls. Our results suggest that IL-33 stimulates ILC2s to secrete IL-13, which, in turn, regulates M-MDSCs to enhance their immune evasion capabilities. Notably, in vitro blockade of IL-33 and IL-13 partially restored the levels and functions of both ILC2s and M-MDSCs. In conclusion, these findings imply that the overactivation of the IL-33-ILC2s-IL-13-M-MDSCs axis may contribute to cervical cancer progression. However, further in vivo blockade studies are required to fully elucidate the precise mechanisms underlying this interaction and to assess its potential therapeutic implications for cervical cancer.
More Related Videos
Related Concept Videos
Cancer Cell Migration through Invadopodia
Induced Pluripotent Stem Cells
Somatic...
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Abnormal Proliferation
The Tumor Microenvironment
Regulation of Hematopoietic Stem Cells

