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Extracellular Granzyme B mediates degradation of Collagen XVII in Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis.
J Invest Dermatol
March 2025
International Collaboration on Repair Discoveries (ICORD) Centre, Vancouver Coastal Health Research Institute, University of British Columbia, Vancouver, BC, Canada; Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada; British Columbia Professional Firefighters' Burn and Wound Healing Group, Vancouver, BC, Canada. Electronic address:
Neutrophil extracellular traps license macrophage production of chemokines to facilitate CD8+ T cell infiltration in obstruction-induced renal fibrosis.
Protein Cell
February 2025
Department of Pediatric Urology, The Seventh Medical Center of Chinese PLA General Hospital, Beijing 100010, China.
Renal fibrosis is a common mechanism leading to kidney failure in chronic kidney diseases (CKDs), including obstructive nephropathy (ON). Dysregulated inflammation is central to the development of renal fibrosis, but how local immune cells within the tissue microenvironment integrate and coordinate to drive this condition remains largely unknown. Herein, we documented that neutrophils were abundantly recruited and expelled neutrophil extracellular traps (NETs) in human and mouse fibrotic kidneys.
View Article and Find Full Text PDFGranzyme K activates the entire complement cascade.
Nature
February 2025
Division of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA, USA.
Granzymes are a family of serine proteases mainly expressed by CD8 T cells, natural killer cells, and innate-like lymphocytes. Although their primary function is thought to be the induction of cell death in virally infected and tumor cells, accumulating evidence indicates certain granzymes can elicit inflammation by acting on extracellular substrates. Recently, we found that the majority of tissue CD8 T cells in rheumatoid arthritis (RA) synovium and in inflamed organs across other diseases express granzyme K (GZMK), a tryptase-like protease with poorly defined function.
View Article and Find Full Text PDFPotential implications of granzyme B in keloids and hypertrophic scars through extracellular matrix remodeling and latent TGF-β activation.
Front Immunol
January 2025
International Collaboration on Repair Discoveries (ICORD) Centre, Vancouver Coastal Health Research Institute (VCHRI), University of British Columbia (UBC), Vancouver, BC, Canada.
Keloid scars (KS) and hypertrophic scars (HS) are fibroproliferative wound healing defects characterized by excessive accumulation of extracellular matrix (ECM) in the dermis of affected individuals. Although transforming growth factor (TGF)-β is known to be involved in the formation of KS and HS, the molecular mechanisms responsible for its activation remain unclear. In this study we investigated Granzyme B (GzmB), a serine protease with established roles in fibrosis and scarring through the cleavage of ECM proteins, as a potential new mediator of TGF-β activation in KS and HS.
View Article and Find Full Text PDFNeutrophil extracellular traps promote growth of lung adenocarcinoma by mediating the stability of m6A-mediated SLC2A3 mRNA-induced ferroptosis resistance and CD8(+) T cell inhibition.
Clin Transl Med
February 2025
The Second Department of Thoracic Oncology, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University/Hunan Cancer Hospital, Changsha, Hunan Province, P.R. China.
To investigate the potential mechanisms underlying neutrophil extracellular traps (NETs) confer ferroptosis resistance and CD8(+) T cell inhibition in lung adenocarcinoma (LUAD). By the intravenous injection of LLC cells into the tail vein, a LUAD mouse model was created. Phorbol-12-myristate-13-acetate (PMA) stimulated neutrophils to facilitate NETs formation and combined with NETs inhibitor DNase I to explore NETs mechanism on LLC cell proliferation, migration, ferroptosis resistance, and CD8(+) T cell activity.
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