No abstract

The placenta is a unique temporary organ essential for growth of the fetus, which determines the success of pregnancy. Its originality relies on a combination of nutritive, endocrine and immunological functions that control maternal immune tolerance to fetus. In the present chapter, we review gene expression programs of placenta from placenta tissue to isolated cells using high throughput transcriptomic approach. Beside trophoblasts, we focused on immune cells including macrophages, dendritic cells and mast cells. From the gene expression signatures, we identify key pathways for the different trimesters of the normal pregnancy and pathological alterations including preeclampsia and gestational diabetes mellitus.

The T cell receptor Vγ9Vδ2 T cells bridge innate and adaptive antimicrobial immunity in primates. These Vγ9Vδ2 T cells respond to phosphoantigens (pAgs) present in microbial or eukaryotic cells in a butyrophilin 3A1 (BTN3) and butyrophilin 2A1 (BTN2A1) dependent manner. In humans, the rapid expansion of circulating Vγ9Vδ2 T lymphocytes during several infections as well as their localization at the site of active disease demonstrates their important role in the immune response to infection. However, Vγ9Vδ2 T cell deficiencies have been observed in some infectious diseases such as active tuberculosis and chronic viral infections. In this review, we are providing an overview of the mechanisms of Vγ9Vδ2 T cell-mediated antimicrobial immunity. These cells kill infected cells mainly by releasing lytic mediators and pro-inflammatory cytokines and inducing target cell apoptosis. In addition, the release of chemokines and cytokines allows the recruitment and activation of immune cells, promoting the initiation of the adaptive immune response. Finaly, we also describe potential new therapeutic tools of Vγ9Vδ2 T cell-based immunotherapy that could be applied to emerging infections.

Observations of vertical transmission of SARS-CoV-2 infection from mother to foetus have recently been described in the literature. However, the consequences of such transmission, whether foetal or neonatal, are poorly understood. From a case of in utero foetal death at 24 +2 weeks of gestation that occurred seven days after the diagnosis of symptomatic SARS-CoV-2 infection in the mother, we isolated the incriminating virus by immunochemistry and molecular techniques in several foetal tissues, with a variant analysis of the SARS-CoV-2 genome. Moreover, the foetal demise could be explained by the presence of placental histological lesions, such as histiocytic intervillositis and trophoblastic necrosis, in addition to foetal tissue damage. We observed mild foetal growth retardation and visceral damage to the liver, causing hepatocellular damage and haemosiderosis. To the best of our knowledge, this is the first report in the literature of foetal demise secondary to maternal-foetal transmission of SARS-CoV-2 with a congenital infection and a pathological description of placental and foetal tissue damage. SARS-CoV-2 was identified in both specimens by three independent techniques (immunochemistry, RT-qPCR and RT-dPCR). Furthermore, the incriminating variant has been identified.