Interleukin (IL)-22 is a member of the IL-10 family of cytokines, which, besides IL-10, contains seven additional cytokines. Although the founding member IL-10 is an important immunoregulatory cytokine that represses both innate and adaptive immunity, the other family members preferentially target epithelial cells and enhance innate host defense mechanisms against various pathogens such as bacteria, yeast, and viruses. Based on their functions, the IL-10 family can be further divided into three subgroups, IL-10 itself, the IL-20 subfamily, and the IFNλ subfamily. IL-22 is the best-studied member of the IL-20 subfamily, and exemplifies the diverse biological effects of this subfamily. IL-22 elicits various innate immune responses from epithelial cells and is essential for host defense against several invading pathogens, including Citrobacter rodentium and Klebsiella pneumonia. IL-22 also protects tissue integrity and maintains the mucosal homeostasis. On the other hand, IL-22 is a proinflammatory cytokine with the capacity to amplify inflammatory responses, which might result in tissue damage, e.g., the IL-22-dependent necrosis of the small intestine during Toxoplasma gondii infection.
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http://dx.doi.org/10.1007/978-3-662-43492-5_10 | DOI Listing |
Front Immunol
January 2025
Institute of Parasitology, Justus Liebig University Giessen, Giessen, Germany.
Bovine besnoitiosis is a re-emerging cattle disease caused by the apicomplexan parasite , which severely affects individual animal welfare and profitability in cattle industry. We recently showed that tachyzoite exposure to bovine polymorphonuclear neutrophils (PMN) effectively triggers neutrophil extracellular trap (NET) formation, leading to parasite immobilization hampering host cell infection. So far, the triggers of this defense mechanism remain unclear.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Physiology, Spinal Cord and Brain Injury Research Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
Spinal cord injury (SCI) leads to permanent motor and sensory loss that is exacerbated by intraspinal inflammation and persists months to years after injury. After SCI, monocyte-derived macrophages (MDMs) infiltrate the lesion to aid in myelin-rich debris clearance. During debris clearance, MDMs adopt a proinflammatory phenotype that exacerbates neurodegeneration and hinders recovery.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Public Health Sciences, College of Medicine, Penn State University, Hershey, PA, USA.
Autoimmune diseases often exhibit a preclinical stage before diagnosis. Electronic health record (EHR) based-biobanks contain genetic data and diagnostic information, which can identify preclinical individuals at risk for progression. Biobanks typically have small numbers of cases, which are not sufficient to construct accurate polygenic risk scores (PRS).
View Article and Find Full Text PDFNat Commun
January 2025
State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing, China.
Potyvirids are the largest group of plant RNA viruses. Pelota, a core component of RNA quality controls (RQC), promotes the degradation of potyvirids' genomic RNA by recognizing a specific GA motif. Here we demonstrate that the viral RNA-dependent RNA polymerase, NIb, acts as a SUMOylation decoy to effectively reduce Pelota SUMOylation by competing with SCE1 to inhibit Pelota-mediated RQC.
View Article and Find Full Text PDFSignal Transduct Target Ther
January 2025
The Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia.
Rampant phospholipid peroxidation initiated by iron causes ferroptosis unless this is restrained by cellular defences. Ferroptosis is increasingly implicated in a host of diseases, and unlike other cell death programs the physiological initiation of ferroptosis is conceived to occur not by an endogenous executioner, but by the withdrawal of cellular guardians that otherwise constantly oppose ferroptosis induction. Here, we profile key ferroptotic defence strategies including iron regulation, phospholipid modulation and enzymes and metabolite systems: glutathione reductase (GR), Ferroptosis suppressor protein 1 (FSP1), NAD(P)H Quinone Dehydrogenase 1 (NQO1), Dihydrofolate reductase (DHFR), retinal reductases and retinal dehydrogenases (RDH) and thioredoxin reductases (TR).
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