Involvement of increased arginase-1 + group 2 innate lymphoid cells and myeloid-derived suppressor cells in endometrial carcinoma: A pilot study
Background
Endometrial carcinoma is a prevalent gynecologic malignancy with a relatively low survival rate. Emerging studies have demonstrated that crosstalk between group 2 innate lymphoid cells (ILC2s) and myeloid-derived suppressor cells drives tumor progression. The immunopathological mechanisms underlying endometrial carcinoma are not yet fully understood.
Methods
This study assessed the frequency of innate lymphoid cells and myeloid-derived suppressor cells as well as related inflammatory mediators in peripheral blood, carcinoma tissue, and para-cancerous tissue of patients with endometrial carcinoma.
Results
Patients with endometrial carcinoma exhibited decreased levels of interleukin-22 and interferon-γ and increased levels of interleukin-25. Infiltration of ILC2s and monocytic myeloid-derived suppressor cells was elevated, while ILC3 levels were reduced. Functional analysis showed enhanced arginase-1 expression in ILC2s obtained from patients with endometrial carcinoma. Both arginase-1 + ILC2s and monocytic myeloid-derived suppressor cells were significantly associated with poorer progression-free survival. A direct correlation between arginase-1 + ILC2s and monocytic myeloid-derived suppressor cells suggests a synergistic role in endometrial carcinoma progression.
Conclusion
Our study indicates that the collaborative effects of ILC2s and myeloid-derived suppressor cells promote type II immunity and may contribute to the progression of endometrial carcinoma. Elevated levels of arginase-1 + ILC2s and monocytic myeloid-derived suppressor cells are associated with a poor prognosis in patients with endometrial carcinoma.