Inflammatory caspases: toward a unified model for caspase activation by inflammasomes
Inflammasomes are inflammatory signaling complexes that provide molecular platforms to
activate the protease function of inflammatory caspases. Caspases-1, -4, -5, and -11 are …
activate the protease function of inflammatory caspases. Caspases-1, -4, -5, and -11 are …
Noncanonical inflammasome signaling elicits gasdermin D–dependent neutrophil extracellular traps
Neutrophil extrusion of neutrophil extracellular traps (NETs) and concomitant cell death (NETosis)
provides host defense against extracellular pathogens, whereas macrophage death …
provides host defense against extracellular pathogens, whereas macrophage death …
[PDF][PDF] Interleukin-1β maturation triggers its relocation to the plasma membrane for gasdermin-D-dependent and-independent secretion
IL-1β requires processing by caspase-1 to generate the active, pro-inflammatory cytokine.
Acute IL-1β secretion from inflammasome-activated macrophages requires caspase-1-…
Acute IL-1β secretion from inflammasome-activated macrophages requires caspase-1-…
An alloy of zinc and innate immunity: Galvanising host defence against infection
JB von Pein, CJ Stocks, MA Schembri… - Cellular …, 2021 - Wiley Online Library
Innate immune cells such as macrophages and neutrophils initiate protective inflammatory
responses and engage antimicrobial responses to provide frontline defence against invading …
responses and engage antimicrobial responses to provide frontline defence against invading …
[PDF][PDF] Class IIa histone deacetylases drive toll-like receptor-inducible glycolysis and macrophage inflammatory responses via pyruvate kinase M2
Histone deacetylases (HDACs) drive innate immune cell-mediated inflammation. Here we
identify class IIa HDACs as key molecular links between Toll-like receptor (TLR)-inducible …
identify class IIa HDACs as key molecular links between Toll-like receptor (TLR)-inducible …
Dimerization and auto-processing induce caspase-11 protease activation within the non-canonical inflammasome
Caspase-11 is a cytosolic sensor and protease that drives innate immune responses to the
bacterial cell wall component, LPS. Caspase-11 provides defence against cytosolic Gram-…
bacterial cell wall component, LPS. Caspase-11 provides defence against cytosolic Gram-…
Caspase-4 dimerisation and D289 auto-processing elicit an interleukin-1β-converting enzyme
…, X Wang, J Acklam, JB Von Pein… - Life Science …, 2023 - life-science-alliance.org
The noncanonical inflammasome is a signalling complex critical for cell defence against
cytosolic Gram-negative bacteria. A key step in the human noncanonical inflammasome …
cytosolic Gram-negative bacteria. A key step in the human noncanonical inflammasome …
Apical extrusion prevents apoptosis from activating an acute inflammatory program in epithelia
K Duszyc, JB von Pein, D Ramnath, D Currin-Ross… - Developmental Cell, 2023 - cell.com
Apoptosis is traditionally considered to be an immunologically silent form of cell death.
Multiple mechanisms exist to ensure that apoptosis does not stimulate the immune system to …
Multiple mechanisms exist to ensure that apoptosis does not stimulate the immune system to …
[HTML][HTML] Modified horseshoe crab peptides target and kill bacteria inside host cells
AS Amiss, JB von Pein, JR Webb, ND Condon… - Cellular and Molecular …, 2022 - Springer
Bacteria that occupy an intracellular niche can evade extracellular host immune responses
and antimicrobial molecules. In addition to classic intracellular pathogens, other bacteria …
and antimicrobial molecules. In addition to classic intracellular pathogens, other bacteria …
Cutting edge: Blockade of inhibitor of apoptosis proteins sensitizes neutrophils to TNF-but not lipopolysaccharide-mediated cell death and IL-1β secretion
The mammalian inhibitor of apoptosis proteins (IAPs) are key regulators of cell death and
inflammation. A major function of IAPs is to block the formation of a cell death–inducing …
inflammation. A major function of IAPs is to block the formation of a cell death–inducing …