<abstract>
<title style='display:none'>Abstract</title>
Pregnancy is a remarkable event where the semi-allogeneic fetus develops in the mother’s uterus, despite genetic and immunological differences. The antigen handling and processing at the maternal–fetal interface during pregnancy appear to be crucial for the adaptation of the maternal immune system and for tolerance to the developing fetus and placenta. Maternal antigen-presenting cells (APCs), such as macrophages (Mφs) and dendritic cells (DCs), are present at the maternal–fetal interface throughout pregnancy and are believed to play a crucial role in this process. Despite numerous studies focusing on the significance of Mφs, there is limited knowledge regarding the contribution of DCs in fetomaternal tolerance during pregnancy, making it a relatively new and growing field of research. This review focuses on how the behavior of DCs at the maternal–fetal interface adapts to pregnancy’s unique demands. Moreover, it discusses how DCs interact with other cells in the decidual leukocyte network to regulate uterine and placental homeostasis and the local maternal immune responses to the fetus. The review particularly examines the different cell lineages of DCs with specific surface markers, which have not been critically reviewed in previous publications. Additionally, it emphasizes the impact that even minor disruptions in DC functions can have on pregnancy-related complications and proposes further research into the potential therapeutic benefits of targeting DCs to manage these complications.
</abstract>

Dendritic Cells and the Establishment of Fetomaternal Tolerance for Successful Human Pregnancy

<abstract>
<title style='display:none'>Abstract</title>
Current therapies for acute radiation syndrome (ARS) involve bone marrow transplantation (BMT), leading to graft-versus-host disease (GvHD). To address this challenge, we have developed a novel donor–recipient chimeric cell (DRCC) therapy to increase survival and prevent GvHD following total body irradiation (TBI)-induced hematopoietic injury without the need for immunosuppression. In this study, 20 Lewis rats were exposed to 7 Gy TBI to induce ARS, and we assessed the efficacy of various cellular therapies following systemic intraosseous administration. Twenty Lewis rats were randomly divided into four experimental groups (<italic>n</italic> = 5/group): saline control, allogeneic bone marrow transplantation (alloBMT), DRCC, and alloBMT + DRCC. DRCC were created by polyethylene glycol-mediated fusion of bone marrow cells from 24 ACI (RT1a) and 24 Lewis (RT11) rat donors. Fusion feasibility was confirmed by flow cytometry and confocal microscopy. The impact of different therapies on post-irradiation peripheral blood cell recovery was evaluated through complete blood count, while GvHD signs were monitored clinically and histopathologically. The chimeric state of DRCC was confirmed. Post-alloBMT mortality was 60%, whereas DRCC and alloBMT + DRCC therapies achieved 100% survival. DRCC therapy also led to the highest white blood cell counts and minimal GvHD changes in kidney and skin samples, in contrast to alloBMT treatment. In this study, transplantation of DRCC promoted the recovery of peripheral blood cell populations after TBI without the development of GVHD. This study introduces a novel and promising DRCC-based bridging therapy for treating ARS and extending survival without GvHD.
</abstract>

Transplantation of Donor–Recipient Chimeric Cells Restores Peripheral Blood Cell Populations and Increases Survival after Total Body Irradiation-Induced Injury in a Rat Experimental Model

<abstract>
<title style='display:none'>Abstract</title>
Endometriosis is a debilitating gynecological disease defined as the presence of endometrium-like epithelium and/or stroma outside the uterine cavity. The most commonly affected sites are the pelvic peritoneum, ovaries, uterosacral ligaments, and the rectovaginal septum. The aberrant tissue responds to hormonal stimulation, undergoing cyclical growth and shedding similar to appropriately located endometrial tissue in the uterus. Common symptoms of endometriosis are painful periods and ovulation, severe pelvic cramping, heavy bleeding, pain during sex, urination and bowel pain, bleeding, and pain between periods. Numerous theories have been proposed to explain the pathogenesis of endometriosis. Sampson’s theory of retrograde menstruation is considered to be the most accepted. This theory assumes that endometriosis occurs due to the retrograde flow of endometrial cells through the fallopian tubes during menstruation. However, it has been shown that this process takes place in 90% of women, while endometriosis is diagnosed in only 10% of them. This means that there must be a mechanism that blocks the immune system from removing endometrial cells and interferes with its function, leading to implantation of the ectopic endometrium and the formation of lesions. In this review, we consider the contribution of components of the Major Histocompatibility Complex (MHC)-I-mediated antigen-processing pathway, such as the ERAP, TAP, LMP, LNPEP, and tapasin, to the susceptibility, onset, and severity of endometriosis. These elements can induce significant changes in MHC-I-bound peptidomes that may influence the response of immune cells to ectopic endometrial cells.
</abstract>

The Antigen-Processing Pathway via Major Histocompatibility Complex I as a New Perspective in the Diagnosis and Treatment of Endometriosis

<abstract>
<title style='display:none'>Abstract</title>
Venous thromboembolism, encompassing acute pulmonary embolism (APE) and deep vein thrombosis (DVT), is a potentially fatal disease with complex pathophysiology. Traditionally, the Virchow triad provided a framework for understanding the pathogenic contributors to thrombus formation, which include endothelial dysfunction, alterations in blood flow and blood hypercoagulability. In the last years, it has become apparent that immunity plays a central role in thrombosis, interacting with classical prothrombotic mechanisms, oxidative stress and vascular factors. Thrombosis amplifies inflammation, and exaggerated inflammatory processes can trigger thrombosis mainly due to the activation of leukocytes, platelets, and endothelial cells. APE-related endothelium injury is a major trigger for immune system activation. Endothelium is also a key component mediating inflammatory reaction and it is relevant to maintain vascular permeability. Exaggerated right ventricular wall stress and overload, with coexisting systemic hypotension and hypoxemia, result in myocardial injury and necrosis. Hypoxia, tissue factor activation and cytokine storm are engaged in the thrombo-inflammatory processes. Thrombus development is characterized by inflammatory state vascular wall caused mainly by an early extravasation of leukocytes and intense selectins and cytokines production. Nevertheless, immunity of DVT is well described, little is known about potential chemokine and cellular differences between thrombus that develops in the vein and thrombus that detaches and lodges in the pulmonary circulation being a cause of APE. There is a paucity of data considering inflammatory state in the pulmonary artery wall during an acute episode of pulmonary embolism. The main aim of this review is to summarize the knowledge of immunity in acute phase of pulmonary embolism in experimental models.
</abstract>

Acute Pulmonary Embolism and Immunity in Animal Models

<abstract>
<title style='display:none'>Abstract</title>
The widespread occurrence of SARS-CoV-2 infections and the diverse range of symptoms have placed significant strain on healthcare systems worldwide. Pregnancy has also been affected by COVID-19, with an increased risk of complications and unfavorable outcomes for expectant mothers. Multiple studies indicate that SARS-CoV-2 can infiltrate the placenta, breach its protective barrier, and infect the fetus. Although the precise mechanisms of intrauterine transmission remain unclear, factors such as perinatal infection, macrophages, sexual intercourse, and the virus’ interaction with host angiotensin-converting enzyme 2 (ACE2) and neuropilin-1 (NRP-1) proteins appear to play a role in this process. The integrity of the placental barrier fluctuates throughout pregnancy and appears to influence the likelihood of fetal transmission. The expression of placental cell receptors, like ACE2, changes during pregnancy and in response to placental damage. However, due to the consistent presence of others, such as NRP-1, SARS-CoV-2 may potentially enter the fetus at different stages of pregnancy. NRP-1 is also found in macrophages, implicating maternal macrophages and Hofbauer cells as potential routes for viral transmission. Our current understanding of SARS-CoV-2's vertical transmission pathways remains limited. Some researchers question the ACE2-associated transmission model due to the relatively low expression of ACE2 in the placenta. Existing studies investigating perinatal transmission and the impact of sexual intercourse have either involved small sample sizes or lacked statistical significance. This review aims to explore the current state of knowledge regarding the potential mechanisms of COVID-19 vertical transmission, identifying areas where further research is needed to fill the gaps in our understanding.
</abstract>

Mechanisms of SARS-CoV-2 Placental Transmission

<abstract>
<title style='display:none'>Abstract</title>
The immune system is regulated by a complex set of genetic, molecular, and cellular interactions. Rapid advances in the study of immunity and its network of interactions have been boosted by a spectrum of “omics” technologies that have generated huge amounts of data that have reached the status of big data (BD). With recent developments in artificial intelligence (AI), theoretical and clinical breakthroughs could emerge. Analyses of large data sets with AI tools will allow the formulation of new testable hypotheses open new research avenues and provide innovative strategies for regulating immunity and treating immunological diseases. This includes diagnosis and identification of rare diseases, prevention and treatment of autoimmune diseases, allergic disorders, infectious diseases, metabolomic disorders, cancer, and organ transplantation. However, ethical and regulatory challenges remain as to how these studies will be used to advance our understanding of basic immunology and how immunity might be regulated in health and disease. This will be particularly important for entities in which the complexity of interactions occurring at the same time and multiple cellular pathways have eluded conventional approaches to understanding and treatment. The analyses of BD by AI are likely to be complicated as both positive and negative outcomes of regulating immunity may have important ethical ramifications that need to be considered. We suggest there is an immediate need to develop guidelines as to how the analyses of immunological BD by AI tools should guide immune-based interventions to treat various diseases, prevent infections, and maintain health within an ethical framework.
</abstract>

Artificial Intelligence, Big Data, and Regulation of Immunity: Challenges and Opportunities

<abstract>
<title style='display:none'>Abstract</title>
The rapid development of nanotechnology has led to the use of silver nanoparticles (Ag-NPs) in various biomedical fields. However, the effect of Ag-NPs on human mesenchymal stem cells (hMSCs) is not fully understood. Moreover, too frequent an exposure to products containing nanosilver in sublethal amounts raises widespread concerns that it will lead to the development of silver-resistant microorganisms. Therefore, this study aimed to evaluate the mechanism of action of Ag-NPs on hMSCs by analyzing the cellular uptake of Ag-NPs by the cells and its effect on their viability and to assess antimicrobial activity of Ag-NPs against emerging bacterial strains, including multidrug-resistant pathogens. For metabolic activity and viability evaluation, hMSCs were incubated with different concentrations of Ag-NPs (14 μg/mL, 7 μg/mL, and 3.5 μg/mL) for 10 min., 1 h and 24 h and subsequently analyzed for their viability by live-dead staining and metabolic activity by the MTS assay. The effect of Ag-NPs on bacterial pathogens was studied by determining their minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC). In conclusion, it was observed that exposure of hMSCs to Ag-NPs of size &lt;10 nm has no cytotoxic effect on the metabolic activity of the cells at the concentration of 3.5 μg/mL, with minimal cytotoxic effect being observed at the concentration of 14 μg/mL after 24 h of incubation. Our findings also confirmed that Ag-NPs at the concentration of 4 μg/mL are effective broad-spectrum bactericidal agents, regardless of the antibiotic-resistance mechanism present in bacteria.
</abstract>

<italic>In Vitro</italic> Effects of Silver Nanoparticles on Pathogenic Bacteria and on Metabolic Activity and Viability of Human Mesenchymal Stem Cells

<abstract>
<title style='display:none'>Abstract</title>
Impaired autophagy, due to the dysfunction of lysosomal organelles, contributes to maladaptive responses by pathways central to the immune system. Deciphering the immune–inflammatory ecosystem is essential, but remains a major challenge in terms of understanding the mechanisms responsible for autoimmune diseases. Accumulating evidence implicates a role that is played by a dysfunctional autophagy–lysosomal pathway (ALP) and an immune niche in psoriasis (Ps), one of the most common chronic skin diseases, characterized by the co-existence of autoimmune and autoinflammatory responses. The dysregulated autophagy associated with the defective lysosomal system is only one aspect of Ps pathogenesis. It probably cannot fully explain the pathomechanism involved in Ps, but it is likely important and should be seriously considered in Ps research. This review provides a recent update on discoveries in the field. Also, it sheds light on how the dysregulation of intracellular pathways, coming from modulated autophagy and endolysosomal trafficking, characteristic of key players of the disease, i.e., skin-resident cells, as well as circulating immune cells, may be responsible for immune impairment and the development of Ps.
</abstract>

Insights into Autophagic Machinery and Lysosomal Function in Cells Involved in the Psoriatic Immune-Mediated Inflammatory Cascade

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