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Mitochondrial sourcing of interferogenic ligands and an autoantigen in human obesity-associated metaflammation.
Obesity (Silver Spring)
September 2023
Translational Research Unit of Excellence, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Objective: Visceral adipose tissue (VAT) inflammation contributes to metabolic dysregulation in obesity. VAT recruitment and activation of plasmacytoid dendritic cells (pDCs) through toll-like receptor 9 (TLR9) recognition of self-DNA, leading to induction of type I interferons, are crucial innate triggers for this VAT inflammation. It was hypothesized that mitochondrial DNA (mtDNA) can contribute to TLR9 activation in VAT-recruited pDCs in obesity, and this study aimed to identify the carrier protein for ligand access to TLR9 and to explore whether this also provides for a source of autoantigens in this context.
View Article and Find Full Text PDFRole of mitochondria in the myopathy of juvenile dermatomyositis and implications for skeletal muscle calcinosis.
J Autoimmun
July 2023
Division of Rheumatology, University of Washington, Seattle, WA, USA. Electronic address:
Article Synopsis
- * Results show that JDM patients have higher mitochondrial markers linked to muscle damage, particularly anti-mitochondrial antibodies, which are associated with calcinosis.
- * The research highlights the role of mitochondrial reactive oxygen species (mtROS) and inflammation in worsening calcification in muscle cells, suggesting potential targets for future therapeutic interventions.
Systemic Lupus Erythematosus Pathogenesis: Interferon and Beyond.
Annu Rev Immunol
April 2023
Drukier Institute for Children's Health and Department of Pediatrics, Weill Cornell Medical Center, New York, NY, USA; email:
Autoreactive B cells and interferons are central players in systemic lupus erythematosus (SLE) pathogenesis. The partial success of drugs targeting these pathways, however, supports heterogeneity in upstream mechanisms contributing to disease pathogenesis. In this review, we focus on recent insights from genetic and immune monitoring studies of patients that are refining our understanding of these basic mechanisms.
View Article and Find Full Text PDFNETs decorated with bioactive IL-33 infiltrate inflamed tissues and induce IFN-α production in patients with SLE.
JCI Insight
November 2021
Laboratory of Rheumatology, Autoimmunity and Inflammation, University of Crete, Medical School, Iraklio, Greece.
IL-33, a nuclear alarmin released during cell death, exerts context-specific effects on adaptive and innate immune cells, eliciting potent inflammatory responses. We screened blood, skin, and kidney tissues from patients with systemic lupus erythematosus (SLE), a systemic autoimmune disease driven by unabated type I IFN production, and found increased amounts of extracellular IL-33 complexed with neutrophil extracellular traps (NETs), correlating with severe, active disease. Using a combination of molecular, imaging, and proteomic approaches, we show that SLE neutrophils, activated by disease immunocomplexes, release IL-33-decorated NETs that stimulate robust IFN-α synthesis by plasmacytoid DCs in a manner dependent on the IL-33 receptor ST2L.
View Article and Find Full Text PDFTLR7 dosage polymorphism shapes interferogenesis and HIV-1 acute viremia in women.
JCI Insight
June 2020
Centre de Physiopathologie de Toulouse Purpan (CPTP), Université de Toulouse, UMR 1043 INSERM, CNRS, Toulouse, France.
Type I IFN (IFN-I) production by plasmacytoid DCs (pDCs) occurs during acute HIV-1 infection in response to TLR7 stimulation, but the role of pDC-derived IFN-I in controlling or promoting HIV-1 infection is ambiguous. We report here a sex-biased interferogenic phenotype for a frequent single-nucleotide polymorphism of human TLR7, rs179008, displaying an impact on key parameters of acute HIV-1 infection. We show allele rs179008 T to determine lower TLR7 protein abundance in cells from women, specifically - likely by diminishing TLR7 mRNA translation efficiency through codon usage.
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