AUTHOR=Zhan Shaowei , Zheng Jing , Zhang Haixia , Zhao Mingdong , Liu Xianbing , Jiang Yuzhu , Yang Chunyan , Ren Liqin , Liu Zhiqiang , Hu Xuemei 

TITLE=LILRB4 Decrease on uDCs Exacerbate Abnormal Pregnancy Outcomes Following Toxoplasma gondii Infection

JOURNAL=Frontiers in Microbiology

VOLUME=9

YEAR=2018

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2018.00588

DOI=10.3389/fmicb.2018.00588

ISSN=1664-302X

ABSTRACT=<p><italic>Toxoplasma gondii</italic> (<italic>T. gondii</italic>) infection in early pregnancy can result in miscarriage, dead fetus, and other abnormalities. The LILRB4 is a central inhibitory receptor in uterine dendritic cells (uDCs) that plays essential immune-regulatory roles at the maternal–fetal interface. In this study, <italic>T. gondii</italic>-infected human primary uDCs and <italic>T. gondii</italic>-infected LILRB4<sup>-/-</sup> pregnant mice were utilized. The immune mechanisms underlying the role of LILRB4 on uDCs were explored in the development of abnormal pregnancy outcomes following <italic>T. gondii</italic> infection <italic>in vitro</italic> and <italic>in vivo</italic>. Our results showed that the expression levels of LILRB4 on uDCs from normal pregnant mice were obviously higher than non-pregnant mice, and peaked in mid-gestation. The LILRB4 expression on uDC subsets, especially tolerogenic subsets, from mid-gestation was obviously down-regulated after <italic>T. gondii</italic> infection and LILRB4 decrease could further regulate the expression of functional molecules (CD80, CD86, and HLA-DR or MHC II) on uDCs, contributing to abnormal pregnancy outcomes. Our results will shed light on the molecular immune mechanisms of uDCs in abnormal pregnancy outcomes by <italic>T. gondii</italic> infection.</p>