Type I interferons are a widely expressed family of effector cytokines that promote innate antiviral and antibacterial immunity. Paradoxically, they can also suppress immune responses by driving production of anti-inflammatory cytokines, and dysregulation of these cytokines can contribute to host-mediated immunopathology and disease progression. Recent studies describe their anti-inflammatory role in intestinal inflammation and the locus containing IFNAR, a heterodimeric receptor for the type I interferons has been identified as a susceptibility region for human inflammatory bowel disease. This review focuses on the role of type I IFNs in the intestine in health and disease and their emerging role as immune modulators. Clear understanding of type I IFN-mediated immune responses may provide avenues for fine-tuning existing IFN treatment for infection and intestinal inflammation.
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http://dx.doi.org/10.1111/imr.12195 | DOI Listing |
ACS Nano
January 2025
Key Lab of Bioorganic Phosphorus Chemistry & Chemical Biology, Department of Chemistry, Tsinghua University, Beijing 100084, China.
As natural agonists of the stimulator of interferon genes (STING) protein, cyclic dinucleotides (CDNs) can activate the STING pathway, leading to the expression of type I interferons and various cytokines. Efficient activation of the STING pathway in antigen-presenting cells (APCs) and tumor cells is crucial for antitumor immune response. Tumor-derived exosomes can be effectively internalized by APCs and tumor cells and have excellent potential to deliver CDNs to the cytoplasm of APCs and tumor cells.
View Article and Find Full Text PDFImmunohorizons
January 2025
Division of Pulmonary Medicine, Department of Pediatrics, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, United States.
Influenza virus infects millions each year, contributing greatly to human morbidity and mortality. Upon viral infection, pathogen-associated molecular patterns activate pattern recognition receptors on host cells, triggering an immune response. The CD209 protein family, homologs of DC-SIGN (dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin), is thought to modulate immune responses to viruses.
View Article and Find Full Text PDFAm J Dermatopathol
January 2025
Department of Dermatology, Brown University, Providence, RI.
Erythromelalgia, a rare cutaneous pain syndrome, is characterized by acral burning pain and flushing, often alleviated by cold and rest. Primary erythromelalgia is caused by gain-of-function mutations of genes encoding for sodium channels, resulting in hyperexcitability of pain signaling neurons. Autoimmunity and hematologic dyscrasias such as thrombocythemia have been implicated in secondary erythromelalgia.
View Article and Find Full Text PDFHeliyon
January 2025
Department of Biotechnology, School of Bio Sciences and Technology, Vellore Institute of Technology, Vellore, 632 014, Tamil Nadu, India.
Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder characterized by the production of autoantibodies, resulting in inflammation and organ damage. Although extensive research has been conducted on SLE pathogenesis, a comprehensive understanding of its molecular landscape in different cell types has not been achieved. This study uncovers the molecular mechanisms of the disease by thoroughly examining gene regulatory networks within neutrophils, dendritic cells, T cells, and B cells.
View Article and Find Full Text PDFActa Physiol (Oxf)
February 2025
UR Diabète et Thérapeutiques, Centre européen d'étude du Diabète, Université de Strasbourg, Strasbourg, France.
Aim: Pancreatic β-cells are susceptible to inflammation, leading to decreased insulin production/secretion and cell death. Previously, we have identified a novel triceps-derived myokine, DECORIN, which plays a pivotal role in skeletal muscle-to-pancreas interorgan communication. However, whether DECORIN can directly impact β-cell function and susceptibility to inflammation remains unexplored.
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