Longsheng Xu1, Ying Zheng1, Jingyu Wang2, Yufen Xu3, Yonghong Xie4, Zhi-Ping Yang5,6. 1. Department of Central Laboratory, The First Affiliated Hospital of Jiaxing University, Jiaxing, China. 2. Department of Pathology, The First Affiliated Hospital of Jiaxing University, Jiaxing, China. 3. Department of Oncology (04-F-14), The First Affiliated Hospital of Jiaxing University, 1882 Zhonghuan South Road, Jiaxing, 314001, China. 4. Department of Pathology, College of Medicine, Jiaxing University, Jiaxing, China. 5. Department of Central Laboratory, The First Affiliated Hospital of Jiaxing University, Jiaxing, China. jxhy7616@163.com. 6. Department of Oncology (04-F-14), The First Affiliated Hospital of Jiaxing University, 1882 Zhonghuan South Road, Jiaxing, 314001, China. jxhy7616@163.com.
Abstract
OBJECTIVE: In this study, we observed the effects of IL-33 on tumor immune response in lung cancer-bearing mice using wild type and MyD88-/- mice respectively. METHODS: Wild C57BL/6 (C57BL/6WT), MyD88 knockout C57BL/6 mice (C57BL/6 MyD88-/-) and Lewis cells were used in this study. Cell proliferation, cytokine release and cytotoxicity were detected. RESULTS: IL-33 could significantly up-regulate specific cellular immunity, inhibit tumor growth and improve survival time in wild type mice group, and it had dose dependent effect. However, IL-33 had no effect on cell immunity and tumor growth in MyD88-/- mice group. Compared with MyD88-/- mice, IL-33 could significantly increase the ratio of CD8+T cells to neutrophils in wild type mice, while the percentage of tumor infiltrating CD11b+ cells, Mo-MDSC, F4/80+ macrophages and mDC cells decreased significantly in wild type mice group. IL-33 could upregulate the expression of CD107a and IFN-γ in CD8+T cells and NK cells of wild type mice, while IL-33 could not upregulate them in MyD88-/- mice. IL-33 could upregulate the expression of CD40, CD80, CD86 and CD205 in DC cells in wild type mice, induce T cells to differentiate into Th1 cells and enhance tumor cell immunity. CONCLUSIONS: IL-33 could promote differentiation and maturation of DC cells through MyD88 pathway, up-regulate the tumor immunity of CD8+T cells and NK cells, and inhibit the proliferation of lung cancer cells.
OBJECTIVE: In this study, we observed the effects of IL-33 on tumor immune response in lung cancer-bearing mice using wild type and MyD88-/- mice respectively. METHODS: Wild C57BL/6 (C57BL/6WT), MyD88 knockout C57BL/6 mice (C57BL/6 MyD88-/-) and Lewis cells were used in this study. Cell proliferation, cytokine release and cytotoxicity were detected. RESULTS:IL-33 could significantly up-regulate specific cellular immunity, inhibit tumor growth and improve survival time in wild type mice group, and it had dose dependent effect. However, IL-33 had no effect on cell immunity and tumor growth in MyD88-/- mice group. Compared with MyD88-/- mice, IL-33 could significantly increase the ratio of CD8+T cells to neutrophils in wild type mice, while the percentage of tumor infiltrating CD11b+ cells, Mo-MDSC, F4/80+ macrophages and mDC cells decreased significantly in wild type mice group. IL-33 could upregulate the expression of CD107a and IFN-γ in CD8+T cells and NK cells of wild type mice, while IL-33 could not upregulate them in MyD88-/- mice. IL-33 could upregulate the expression of CD40, CD80, CD86 and CD205 in DC cells in wild type mice, induce T cells to differentiate into Th1 cells and enhance tumor cell immunity. CONCLUSIONS:IL-33 could promote differentiation and maturation of DC cells through MyD88 pathway, up-regulate the tumor immunity of CD8+T cells and NK cells, and inhibit the proliferation of lung cancer cells.
Entities:
Keywords:
CD8+T cell; DC cell; IL-33; Lung cancer; NK cell
Authors: Abrar Ul Haq Khan; Saeedah Musaed Almutairi; Alaa Kassim Ali; Rosalba Salcedo; C Andrew Stewart; Lisheng Wang; Seung-Hwan Lee Journal: Front Immunol Date: 2021-05-03 Impact factor: 7.561