Jun-Ying Cai1, Mu-Jun Li2. 1. Department of Reproductive Center, First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi Province, China. Electronic address: caijunying2012@126.com. 2. Department of Reproductive Center, First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi Province, China. Electronic address: lmj20051699@126.com.
Abstract
BACKGROUND: This study investigated the effects of interleukin 23 (IL-23) on the production of cytokines (IL-1, IL-4, IL-10, and IL-17), the differentiation of Treg/Th17 and STAT3 (i.e., signal transducer and activator of transcription 3) in human decidual immune cells (DICs) during early pregnancy. METHODS: DICs were treated with recombinant human IL-23 and an antibody against IL-23 subunit p19. The differentiation of Treg and Th17 cells was detected by flow cytometry. Levels of IL-23 receptor (IL-23R), STAT3, and phosphorylated STAT3 (pSTAT3) was examined by Western blot. The production of IL1, IL4, IL10, and IL-17 in DICs was measured by ELISA. RESULTS: Exogenous recombinant human IL-23 significantly promoted the differentiation of Th17 cells from DICs, while anti-IL-23 antibody significantly promoted the differentiation of Treg cells from DICs. Consistent with the differentiation of Th17 and Tregs cells, levels of IL-1β and IL-17 correlated positively with IL-23 treatment, and anti-IL-23 antibody increased the secretion of IL-4 and IL-10 from DICs. Levels of pSTAT3, but not STAT3 or IL-23R, were significantly elevated by recombinant IL-23 treatment; anti-IL-23 antibody significantly decreased the levels of pSTAT3 and IL-23R in DICs. CONCLUSIONS: IL-23 mediates the differentiation of Th17 and Treg cells and the production of associated cytokines in DICs. The potential mechanism likely involves the STAT3 pathway.
BACKGROUND: This study investigated the effects of interleukin 23 (IL-23) on the production of cytokines (IL-1, IL-4, IL-10, and IL-17), the differentiation of Treg/Th17 and STAT3 (i.e., signal transducer and activator of transcription 3) in human decidual immune cells (DICs) during early pregnancy. METHODS: DICs were treated with recombinant humanIL-23 and an antibody against IL-23 subunit p19. The differentiation of Treg and Th17 cells was detected by flow cytometry. Levels of IL-23 receptor (IL-23R), STAT3, and phosphorylated STAT3 (pSTAT3) was examined by Western blot. The production of IL1, IL4, IL10, and IL-17 in DICs was measured by ELISA. RESULTS: Exogenous recombinant humanIL-23 significantly promoted the differentiation of Th17 cells from DICs, while anti-IL-23 antibody significantly promoted the differentiation of Treg cells from DICs. Consistent with the differentiation of Th17 and Tregs cells, levels of IL-1β and IL-17 correlated positively with IL-23 treatment, and anti-IL-23 antibody increased the secretion of IL-4 and IL-10 from DICs. Levels of pSTAT3, but not STAT3 or IL-23R, were significantly elevated by recombinant IL-23 treatment; anti-IL-23 antibody significantly decreased the levels of pSTAT3 and IL-23R in DICs. CONCLUSIONS:IL-23 mediates the differentiation of Th17 and Treg cells and the production of associated cytokines in DICs. The potential mechanism likely involves the STAT3 pathway.