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Preeclampsia is a syndrome with multiple etiologies. The diagnosis can be made without proteinuria in the presence of dysfunction of at least 1 organ associated with hypertension. The common pathophysiological pathway includes endothelial cell activation, intravascular inflammation, and syncytiotrophoblast stress. There is evidence to support, among others, immunologic causes of preeclampsia. Unlike defense immunology, reproductive immunology is not based on immunologic recognition systems of self/non-self and missing-self but on immunotolerance and maternal–fetal cellular interactions. The main mechanisms of immune escape from fetal to maternal immunity at the maternal–fetal interface are a reduction in the expression of major histocompatibility complex molecules by trophoblast cells, the presence of complement regulators, increased production of indoleamine 2,3-dioxygenase, activation of regulatory T cells, and an increase in immune checkpoints. These immune protections are more similar to the immune responses observed in tumor biology than in allograft biology. The role of immune and nonimmune decidual cells is critical for the regulation of trophoblast invasion and vascular remodeling of the uterine spiral arteries. Regulatory T cells have been found to play an important role in suppressing the effectiveness of other T cells and contributing to local immunotolerance. Decidual natural killer cells have a cytokine profile that is favored by the presence of HLA-G and HLA-E and contributes to vascular remodeling. Studies on the evolution of mammals show that HLA-E, HLA-G, and HLA-C1/C2, which are expressed by trophoblasts and their cognate receptors on decidual natural killer cells, are necessary for the development of a hemochorial placenta with vascular remodeling. The activation or inhibition of decidual natural killer cells depends on the different possible combinations between killer cell immunoglobulin-like receptors, expressed by uterine natural killer cells, and the HLA-C1/C2 antigens, expressed by trophoblasts. Polarization of decidual macrophages in phenotype 2 and decidualization of stromal cells are also essential for high-quality vascular remodeling. Knowledge of the various immunologic mechanisms required for adequate vascular remodeling and their dysfunction in case of preeclampsia opens new avenues of research to identify novel biological markers or therapeutic targets to predict or prevent the onset of preeclampsia.

Background. The humoral response to SARS-CoV-2 infection in hemodialysis patients needs to be clarified. Methods. In this retrospective study performed in two dialysis facilities, we measured the circulating levels of SARS-CoV-2 antibodies in patients who were on maintenance hemodialysis during the first wave of the epidemic in March and April 2020 and were still alive 6 months later. We also investigated associations between the patients diagnosed as infected during the first wave and several clinical, biological, and radiological parameters of COVID-19. Finally, we compared these circulating levels of SARS-CoV-2 antibodies with those of a control group of healthcare workers infected during the same period. Results. Of the 299 hemodialysis patients who recovered from the first wave of the epidemic 6 months before, 59 had a positive SARS-CoV-2 antibody whereas only 45 patients were diagnosed as infected during the first wave of the epidemic. All infected hemodialysis patients developed circulating antibodies. Using a clustering method, a significant correlation was identified between the cluster with the lowest circulating levels of SARS-CoV-2 antibodies and the severity of COVID-19 based on several parameters including CRP, BNP, lymphocyte count, neutrophil-lymphocyte ratio, and oxygen requirements, as well as pulmonary involvement on chest scan. Moreover, the circulating levels of the SARS-CoV-2 antibodies in surviving hemodialysis patients (n = 59) were similar to those of the control group (n = 17). Conclusion. The main finding of this study is that all of the surviving hemodialysis patients who were diagnosed with SARS-CoV-2 infection from March to April 2020 developed a persistent humoral response with significant circulating levels of SARS-CoV-2 antibodies, 6 months later. Another important finding is that surviving hemodialysis patients who had more severe disease had lower circulating levels of SARS-CoV-2 antibodies. Finally, circulating levels of SARS-CoV-2 antibodies were similar in surviving hemodialysis patients and healthcare workers without kidney disease.