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In mammalian species, pregnancy is a complex process that involves the maternal recognition of pregnancy, implantation, decidualization, placentation, and parturition. The innate immune system is composed of cellular components, such as natural killer cells, neutrophils, monocytes, and macrophages, and effector molecules, such as cytokines, interferons, antimicrobial peptides, and complement components. The innate immune system plays a critical role as the first line of defense against infection or inflammation to maintain homeostasis and activate the adaptive immunity. During pregnancy, innate immune cells and effector molecules act on the regulation of innate immunity for host defense and processes such as embryo development, implantation, and placentation at the maternal-conceptus interface. In this review, we describe the components of the innate immune system and their functions at the maternal-conceptus interface to establish and maintain pregnancy in animal species that form hemochorial- or epitheliochorial-type placentas, including humans, rodents, ruminants, and pigs.
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http://dx.doi.org/10.5713/ab.24.0257 | DOI Listing |
Natl Sci Rev
September 2025
School of Life Science, Beijing University of Chinese Medicine, Beijing 100029, China.
The role of cholesterol metabolism in antiviral immunity has been established, but if and how this cholesterol-mediated immunometabolism can be regulated by specific small molecules is of particular interest in the quest for novel antiviral therapeutics. Here, we first demonstrate that NPC1 is the key cholesterol transporter for suppressing viral replication by changing cholesterol metabolism and triggering the innate immune response via systemic analyses of all possible cholesterol transporters. We then use the Connectivity Map (CMap), a systematic methodology for identifying functional connections between genetic perturbations and drug actions, to screen NPC1 inhibitors, and found that bis-benzylisoquinoline alkaloids (BBAs) exhibit high efficacy in the inhibition of viral infections.
View Article and Find Full Text PDFFront Cell Infect Microbiol
September 2025
Universidad Autónoma de Nuevo León, Servicio y Departamento de Inmunología, Facultad de Medicina, Monterrey, NL, Mexico.
Natural killer (NK) cells are innate lymphocytes with cytotoxic activity against tumors and viruses. The pandemic of the coronavirus disease 2019 (COVID-19) has increased the investigation of their role in disease severity. However, their functional status and modulators remain controversial.
View Article and Find Full Text PDFImmunooncol Technol
September 2025
Division of Tumor Biology & Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Background: Breast cancer is a systemic disease, yet the impact of tumor molecular subtype and disease stage on the systemic immune landscape remains poorly understood. In this study, we comprehensively analyzed the systemic immune landscape in a large cohort of breast cancer patients, encompassing all molecular subtypes and disease stages, alongside a control group of healthy donors.
Materials And Methods: Using multi-parameter flow cytometry, we assessed the abundance, phenotype, and activation status of diverse innate and adaptive immune cell populations across peripheral blood samples from 355 breast cancer patients and 65 healthy donors.
Rev Cardiovasc Med
August 2025
Henan Key Laboratory of Medical Tissue Regeneration, Xinxiang Medical University, 453003 Xinxiang, Henan, China.
Myocarditis is a life-threatening inflammatory disorder that affects the cardiac muscle tissue. Current treatments merely regulate heart function but fail to tackle the root cause of inflammation. In myocarditis, the initial wave of inflammation is characterized by the presence of neutrophils.
View Article and Find Full Text PDFCell Physiol Biochem
September 2025
Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institute of Biochemistry, 10117 Berlin, Germany.
Background/aims: The ubiquitin-like protein ISG15 and its covalent conjugation to substrates (ISGylation) represent a critical interferon (IFN)-induced antiviral mechanism. USP18 is an ISG15-specific isopeptidase and a key negative regulator of type I IFN signaling. While inactivation of USP18's catalytic activity enhances ISGylation and promotes viral resistance, its role in modulating inflammation and cardiac function during CVB3-induced myocarditis remains unclear.
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