Changes of Inhibitory Receptors on NK-92 Cells and HLA-G on BeWo Cells with Toxoplasma gondii Infection
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Changes of Inhibitory Receptors on NK-92 Cells and HLA-G on BeWo Cells with Toxoplasma gondii Infection Yang Liu,1 Ling Zhang,1 Meilan Gao,2 Fengmei Zhang,3 Xiaoyan Xu,1 Xianbing Liu,1 and Xuemei Hu1,4
Abstract—The aim of this study were to demonstrate the effects of Yellow fluorescent proteinToxoplasma gondii infection on the NK-92 cells co-cultured with BeWo cells in vitro and to verify the implications upon adverse pregnancy outcome. There are four groups including NK-92 cells infected or uninfected with T. gondii, and NK-92 cells co-cultured with BeWo cells in the presence or absent of T. gondii infection. Cells were observed by fluorescence microscope at 12, 24, 36, 48, and 60 h after infection. Levels of inhibitory receptors killer immunoglobulin-like receptor (KIR)2DL4 and ILT-2 expressed on NK-92 cells, and their common ligand HLA-G expressed on BeWo cells were measured by real-time PCR and flow cytometry in all groups. Levels of KIR2DL4, ILT-2 and HLA-G increased at 12, 24, 36, and 48 h, while decreased at 60 h in all T. gondii-infected groups compared with their parallel control groups, respectively. KIR2DL4 and ILT-2 expression in co-culture groups with infection were higher than those in infected NK-92 groups at 12, 24, 36, and 48 h, while there were no significant differences at 60 h. The expression of the two inhibitory receptors was correlated with HLA-G expression in infected co-culture groups. The changes of inhibitory receptors on NK-92 cells and their common ligand HLA-G on BeWo cells with T. gondii infection might contribute to the occurrence of adverse pregnancy outcome. KEY WORDS: Toxoplasma gondii; HLA-G; KIR2DL4; ILT-2; adverse pregnancy outcome.
INTRODUCTION Toxoplasma gondii, a zoonotic pathogen of toxoplasmosis, is one of the pathogens of human TORCH syndrome that can infect all warm-blooded animals [1, 2]. T. gondii infection is generally asymptomatic among humans and animals with normal immunity, but it can cause a high level of morbidity and mortality in immunocompromised inYang Liu and Ling Zhang contributed equally to this work. 1
Department of Immunology, Binzhou Medical University, No.346 Guan-Hai Road, Lai-shan, Yantai, Shandong 264003, People’s Republic of China 2 Department of Clinical Laboratory, Binzhou Affiliated Hospital of Binzhou Medical University, Binzhou, Shandong 264003, People’s Republic of China 3 School Hospital, Binzhou Medical University, Yantai, Shandong 264003, People’s Republic of China 4 To whom correspondence should be addressed at Department of Immunology, Binzhou Medical University, No.346 Guan-Hai Road, Lai-shan, Yantai, Shandong 264003, People’s Republic of China. Email: [email protected]
dividuals. Specifically, if a primary infection with T. gondii occurs during human pregnancy, particularly during the first trimester, it can cause unfavorable pregnancy outcomes such as miscarriage, stillbirth, or fetal abnormalities [3, 4]. However, the mechanism by which T. gondii infection causes these severe abnormalities during human pregnancy remains unclear. Under no
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