Cited by 371Inflammasome and immune disordersImmune Response and InflammationCell death mechanisms and regulation

NLRs at the intersection of cell death and immunity

Ting, Jenny P.-Y., Willingham, Stephen B., Bergstralh, Daniel T.·2008·Nature Reviews Immunology

Abstract

Inflammation is a crucial element of the host response to cellular insult. Pathogen-induced inflammation includes a molecular pathway which proceeds through activation of the protease caspase-1 to the release of the inflammatory cytokines interleukin-1 (IL-1) and IL-18. Importantly, pathogens may also induce forms of cell death that have inherently pro-inflammatory features. Here, we review recent evidence demonstrating that NLR (nucleotide-binding domain, leucine-rich repeat containing) family proteins serve as a common component of both caspase-1-activated apoptotic pathways and caspase-independent necrotic pathways. Parallels are drawn between NLR protein function and the activity of structurally similar proteins involved in cell death: the apoptotic mediator APAF1 (apoptotic-protease-activating factor 1) and the plant disease resistance NBS-LRR (nucleotide-binding site leucine-rich repeats) proteins.

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Crossref · 10.1038/nri2296

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  • Polynucleotides and oligonucleotides from degrading DNA or RNA can act on TLR3, TLR7, TLR8, or TLR9 and on intracellular receptors RIG1, MDA5, or LGP2, while ATP and its degradation products may activate or inhibit distinct classes of purinergic receptors.

    “Polynucleotides and oligonucleotides derived from degrading DNA or RNA can act on TLR3, TLR7, TLR8, or TLR9 as well as on intracellular receptors including RIG1, MDA5, or LGP2, while ATP and its degradation products may activate or inhibit distinct classes of purinergic receptors 45,108,109.”

    From Immunogenic and tolerogenic cell death (2009) · cites this paper as [108]

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Authors
Ting, J. P.-Y., Willingham, S. B., & Bergstralh, D. T.
Affiliations
University of North Carolina at Chapel Hill (US)
Corresponding author
Ting, Jenny P.-Y.
Venue
Nature Reviews Immunology
Published
2008-05
Volume
8
Issue
5
Pages
372-379
ISSN
  • 1474-1733 (ISSN-L)
  • 1474-1741
OpenAlex
W2050870561
Cited by
371
References
145
Citations by year
2026: 5 · 2025: 9 · 2024: 7 · 2023: 8 · 2022: 10 · 2021: 14 · 2020: 10 · 2019: 19 · 2018: 18 · 2017: 18 · 2016: 17 · 2015: 19 · 2014: 22 · 2013: 27 · 2012: 36
FWCI
3.40
Type
journal article
Language
en
Open access
closed
Locations
  • Nature reviews. Immunology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
NLR proteins, cell death, pyroptosis, caspase-1, apoptosis, necrosis, inflammation, interleukin-1, IL-18, Apaf-1, NBS-LRR proteins, plant disease resistance, host-pathogen interaction
MeSH terms
NLR Proteins, Leucine-Rich Repeat Proteins, Animals, Communicable Diseases, Humans, Interleukin-1, Necrosis, Proteins, Tumor Necrosis Factor-alpha, Apoptosis, Caspase 1, HMGB1 Protein, Intracellular Signaling Peptides and Proteins, Adaptor Proteins, Signal Transducing, Apoptosis Regulatory Proteins, Apoptotic Protease-Activating Factor 1

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