Plasmacytoid dendritic cells (pDCs) are key players in the antiviral immune response and type III IFNs such as IL-29 appear to play a pivotal role in pDC function. Pronounced susceptibility to viral infections in neonates is partly resulting from diminished antiviral immune mechanisms. Accordingly, the aim of the present study was to investigate the impact of IL-29 in the altered immune response of neonatal pDCs. PBMCs of adult and term newborns were stimulated with CpG-ODN2216 in the presence or absence of IL-29 and assessed for IFN-α production, downstream-signaling, and activation marker expression. A significantly lower IL-29 production after TLR9-specific stimulation was demonstrated in neonatal pDCs. IL-29 enhanced the IFN-α production of pDCs in adults compared to newborns. Newborn pDCs displayed a significantly lower surface expression of IL-10 and IL-28Rα receptor resulting in diminished STAT1 and IRF7 activation. Interestingly, concomitant stimulation with CpG-ODN2216/IL-29 had no impact on the expression of surface activation and maturation markers of pDCs in neither population. The diminished antiviral immune response of neonatal pDCs is associated with reduced production and cellular responses toward IL-29. Potential therapeutic agents enhancing the IL-29 response in neonatal pDCs possibly augment viral protection in newborns.
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http://dx.doi.org/10.1002/JLB.4A0518-189R | DOI Listing |
Cardiovasc Res
January 2025
Department of Pathophysiology, Shenzhen University Medical School, Shenzhen 518060, China.
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View Article and Find Full Text PDFAntioxid Redox Signal
January 2025
Department of Physiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.
Hypoxia ischemia (HI) is a leading cause of cerebral palsy and long-term neurological sequelae in infants. Given that mitochondrial dysfunction in neurons contributes to HI brain damage, this study aimed to investigate the regulatory role of miR-9-5p in mitochondrial function following HI injury. Overexpression of miR-9-5p in HI mice or HO-exposed PC12 cells suppressed neuronal injury, associated with increased mitochondrial copy number, normalizing mitochondrial membrane potential, improved nuclear factor-erythroid factor 2-related factor 2 (Nrf2) activation, and downregulation of Keap1.
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January 2025
Laboratorio de Pediatria Clinica (LIM36), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil.
Introduction: Chemokines and their receptors are essential for leukocyte migration to several tissues, including human milk. Here, we evaluated the homing of T and B lymphocyte subsets to breast milk in response to ongoing respiratory infections in the nursing infant.
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Int J Pept Res Ther
January 2025
Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, United States 46202.
Purpose: Heterozygous mutations in the insulin gene can give rise to a monogenic diabetes syndrome due to toxic misfolding of the variant proinsulin in the endoplasmic reticulum (ER) of pancreatic β-cells. Clinical mutations are widely distributed in the sequence (86 amino acids). Misfolding induces chronic ER stress and interferes in with wildtype biosynthesis and secretion.
View Article and Find Full Text PDFEur J Pharmacol
January 2025
Department of Basic Medicine, Institute of Respiratory Diseases Xiamen Medical College, Xiamen Medical College, Xiamen, Fujian 361023, P. R. China; State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Harbin Medical University, Harbin, Heilongjiang 150081, P. R. China. Electronic address:
ITFG2 is an intracellular protein known to modulate the immune response of T-cells. Our previous investigation revealed that ITFG2 specifically targets ATP5b to regulate ATP energy metabolism and maintain mitochondrial function, thereby protecting the heart from ischemic injury. However, the role of ITFG2 in ischemic ventricular arrhythmias and its underlying mechanisms have not been previously reported.
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