Deleterious molecules or factors produced by pathogens can hinder the normal physiological functioning of organisms. In response to these survival challenges, organisms rely on innate immune signaling as their first line of defense, which regulates immune-responsive genes and antimicrobial peptides to protect against pathogenic infections. These genes are under the control of transcription factors, which are known to regulate the transcriptional activity of genes after binding to their regulatory sequences. Previous studies have employed as a host-pathogen interaction model to demonstrate the essential role of different transcription factors in the innate immunity of worms. In this review, we summarize the advances made regarding the functioning of distinct transcription factors in the innate immune response upon pathogen infection. Finally, we discuss the open questions in the field, whose resolutions have the potential to expand our understanding of the mechanisms underlying the innate immunity of organisms.
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http://dx.doi.org/10.3390/cells14050327 | DOI Listing |
J Immunol
January 2025
Key Laboratory of Breeding Biotechnology and Sustainable Aquaculture, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, P. R. China.
The von Hippel-Lindau (VHL) tumor suppressor gene VHL is a classic tumor suppressor that has been identified in family members with clear cell renal cell carcinomas, central nervous system and retinal hemangioblastomas, phaeochromocytomas, and pancreatic neuroendocrine tumors. The well-defined function of VHL is to mediate proteasomal degradation of hydroxylated hypoxia-inducible factor α proteins, resulting in the downregulation of hypoxia-responsive gene expression. Previously, we reported that VHL inhibits antiviral signaling by targeting mitochondrial antiviral signaling protein (MAVS) for proteasomal degradation.
View Article and Find Full Text PDFJ Immunol
February 2025
Department of Pharmacology and Toxicology, University of Arizona, Tucson, AZ, United States.
Mitochondrial antiviral-signaling protein (MAVS) is a key adapter protein required for inducing type I interferons (IFN-Is) and other antiviral effector molecules. The formation of MAVS aggregates on mitochondria is essential for its activation; however, the regulatory mitochondrial factor that mediates the aggregation process is unknown. Our recent work has identified the protein Aggregatin as a critical seeding factor for β-amyloid peptide aggregation.
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March 2025
School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104 United States.
Interleukin 33 (IL-33) is a pleiotropic cytokine released from diverse cell types that regulate both pro- and anti-inflammatory responses during pathogen infection. However, it remains unclear whether IL-33 controls key aspects of cutaneous immunity against skin-penetrating parasites. In this study, mice percutaneously infected with the parasitic helminth Strongyloides ratti were investigated to understand mechanisms of anamnestic immunity at the skin barrier.
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February 2025
Division of Infectious Diseases, Vanderbilt University Medical Center, Nashville, TN, United States.
Persistent systemic inflammation is associated with an elevated risk of cardiometabolic diseases. However, the characteristics of the innate and adaptive immune systems in individuals who develop these conditions remain poorly defined. Doublets, or cell-cell complexes, are routinely eliminated from flow cytometric and other immune phenotyping analyses, which limits our understanding of their relationship to disease states.
View Article and Find Full Text PDFJ Immunol
March 2025
Department of Veterinary and Animal Sciences, University of Massachusetts Amherst, Amherst, MA, United States.
Alveolar macrophages (AMs) are lung-resident myeloid cells and airway sentinels for inhaled pathogens and environmental particles. While AMs can be highly inflammatory in response to respiratory viruses, they do not mount proinflammatory responses to all airborne pathogens. For example, we previously showed that AMs fail to mount a robust proinflammatory response to Mycobacterium tuberculosis.
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