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Updated: Jun 16, 2025
Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
Published on: May 21, 2018
NLRP3 inflammasome: From drug target to drug discovery
Ling Yin1, Hongliang Zhang2, Yuhua Shang3
1Center of Disease Immunity and Intervention, College of Medicine, Lishui University, Lishui 323000, China; College of Medicine, University of Florida, Gainesville, FL 32608, USA; Division of Infectious Diseases and Geographic Medicine, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Laboratory of Structural Immunology, Key Laboratory of Immune Response and Immunotherapy, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230027 China; Institute of Health and Medicine, Hefei Comprehensive National Science Center, Hefei, Anhui, China.
Abstract:
The immune system employs innate and adaptive immunity to combat pathogens and stress stimuli. Innate immunity rapidly detects pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) via pattern recognition receptors (PRRs), whereas adaptive immunity mediates antigen-specific T/B cell responses. The NLRP3 inflammasome, a key cytoplasmic PRR, consists of leucine-rich repeat, nucleotide-binding, and pyrin domains. Its activation requires priming (signal 1: Toll-like receptors/NOD-like receptors/cytokine receptors) and activation (signal 2: PAMPs/DAMPs/particulates). NLRP3 triggers cytokine storms and neuroinflammation, contributing to inflammatory diseases. Emerging therapies target NLRP3 via nuclear receptors (transcriptional regulation), adeno-associated virus (AAV) vectors (gene delivery), and microRNAs (post-transcriptional modulation). This review highlights NLRP3's signaling cascade, pathological roles, and combinatorial treatments leveraging nuclear receptors, AAVs, and microRNAs for immunomodulation.
