Inflammation Initiation Complex

Inflammasomes & Inflammatory Diseases

Inflammasomes, first identified in 2002, are signaling platforms that mediate pathological inflammation and tissue damage.

NLRP3 In CNS Inflammation: Neutrophils And BBB

NLRP3 is a cytosolic inflammasome sensor that assembles with ASC and caspase-1 after priming and activation signals.

cGAS-STING Pathway: Biology, Activation, And Signaling

The cGAS-STING pathway detects double-stranded DNA in inappropriate cellular locations and converts it into innate immune signaling.

Interleukins: Mechanisms Of Dual Effects In Inflammation

Interleukins are a diverse cytokine group that coordinates host defense, hematopoiesis, metabolism, tissue repair, and adaptive immunity.

Molecular And Cellular Mechanisms Underlying Alveolar Bone Loss In Periodontitis

Periodontitis is a chronic immunoinflammatory disease in which a dysbiotic biofilm and a susceptible host response destroy gingiva, periodontal ligament, cementum, and alveolar bone.

The Core Of Inflammatory Stress: The Apoptosome, Inflammasome, And PIDDosome

The apoptosome, inflammasome, and PIDDosome are supramolecular caspase-activation platforms that translate cellular stress into apoptosis, inflammation, cell-cycle control, or differentiation.

Significance Of Cytokine Polymerization And Its Association With Disease Progression

“Cytokine polymerization” is not a standardized umbrella mechanism in current inflammation biology.

Mitochondria-Mediated Inflammation Associated with Cell Death

Mitochondria-mediated inflammation links metabolic organelle damage to innate immune sensing and cell-death outcome.

Pattern Recognition Receptors for Pathogen Detection

Pattern recognition receptors (PRRs) are germline-encoded sensors that detect conserved microbial structures and signals of cellular damage, converting recognition into innate defense and instruction of adaptive immunity.

Inflammasome Pathways Overview

Inflammasomes are cytosolic multiprotein platforms that convert microbial or cellular danger detection into inflammatory caspase activation, IL-1β and IL-18 maturation, and often gasdermin-dependent pyroptosis.

Complexity of Cell Death-Induced Inflammation

Cell death-induced inflammation is not a fixed property of one death morphology.

Pyroptosis, PANoptosis, and Immunity

Pyroptosis is a lytic inflammatory death program executed by gasdermin pores, whereas PANoptosis describes coordinated inflammatory death with pyroptotic, apoptotic, and necroptotic components that cannot be explained by any one pathway alone.

Phagoptosis: Cell Death via Phagocytosis

Phagoptosis is death caused by engulfment of a cell that was viable when phagocytosis began.

Dual immune-driven atherosclerosis

Dual immune-driven atherosclerosis reflects the coordinated contribution of innate and adaptive immunity to lipid-rich arterial disease.

Health Risks and Drivers of Clonal Hematopoiesis

Clonal hematopoiesis is the expansion of a blood-cell clone carrying an acquired mutation or chromosomal alteration.

Antiphospholipid antibodies and cardiovascular thrombosis

Antiphospholipid antibodies are persistent autoantibodies directed against phospholipids or phospholipid-binding proteins, principally lupus anticoagulant, anticardiolipin, and anti-β2-glycoprotein I.

"Blood Metabolism" and the Inhibition of Pathological Transformation in Atherosclerosis

In atherosclerosis, “blood metabolism” is most usefully interpreted as the metabolic programming of circulating and plaque-resident immune cells and their progenitors.

Association between the procoagulant pathway and thromboinflammation.

Thromboinflammation describes pathological reinforcement between innate immunity, platelet activation, endothelial responses, and coagulation.

Mechanisms Linking Autoimmunity to Cardiovascular Disease

Autoimmunity increases cardiovascular risk through immune mechanisms that overlap with, but are not explained by, hypertension, dyslipidemia, and other conventional risk factors.

Floatptosis: Lysosomal Fusion-Associated Termination Of Cell Death

Floatptosis is a newly reported cytoplasmic vacuolization cell death pathway defined as 'Fused LysosOme-Associated Termination' in macrophages infected by a Bergeyella cardium variant.

Characteristic Interleukin Family Cytokines In Various Inflammatory Models

Interleukin family cytokines define inflammatory models because they translate tissue injury, infection, barrier stress, and immune-cell activation into recognizable cytokine signatures.

The Interaction Between Inflammageing And Clonal Hematopoiesis And Its Impact On Disease

Inflammageing and clonal hematopoiesis form a self-reinforcing axis in aging biology.

The STING-NF-κB Anti-Infection Signaling Cascade

STING-NF-κB anti-infection signaling describes a cytosolic DNA-sensing cascade that links microbial DNA detection to inflammatory cytokine production and host defense.

Regulation of Type I Interferon in the Prevention and Treatment of Viral and Inflammatory Diseases

Regulation of type I interferon in the prevention and treatment of viral and inflammatory diseases refers to the control of interferon-α and interferon-β production, signaling, and biological activity to balance antiviral defense with immune homeostasis.

How NF-κB Writes Inflammatory Memory

How NF-κB writes inflammatory memory refers to the capacity of NF-κB signaling to convert transient inflammatory stimuli into persistent transcriptional, epigenetic, and cellular states that influence future immune responses.

Trained Immunity: Innate Immune Memory in Inflammation and Disease

Trained immunity refers to the capacity of the innate immune system to develop a long-term altered response following exposure to microbial products, vaccines, or endogenous danger signals, resulting in enhanced responsiveness to subsequent heterologous challenges.

The Guiding Significance of Erythrocyte "Spectosis".

Spectosis is a lytic programmed cell death pathway in mature red blood cells triggered by complement activation and involving NLRP3 signaling.

Neutrophil Extracellular Traps & Inflammatory Diseases

Neutrophil extracellular traps (NETs) are extracellular web-like structures composed of decondensed chromatin and antimicrobial proteins that were originally identified as a mechanism by which neutrophils capture and eliminate pathogens.