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NOD-like receptors: major players (and targets) in the interface between innate immunity and cancer

Fernando J Velloso1,2, Marina Trombetta-Lima2, Valesca Anschau3

  • 1Department of Pharmacology, Physiology and Neuroscience, Rutgers-New Jersey Medical School Newark, NJ, U.S.A. fernando.velloso@rutgers.edu rcorrea@sbpdiscovery.org.

Bioscience Reports
|March 7, 2019
PubMed

Insights

Pattern recognition receptors (PRRs), including NLRs, detect pathogens and tissue injury. Dysregulated NLR signaling promotes inflammation and human cancers, highlighting their crucial role in disease.

Area of Science:

  • Immunology
  • Molecular Biology
  • Oncology

Background:

  • Innate immunity relies on pattern recognition receptors (PRRs) to detect pathogens and cellular damage.
  • NLRs (NACHT and Leucine-Rich Repeat domain containing proteins) are key cytosolic PRRs sensing intracellular threats.
  • NLR signaling pathways are critical for host defense but can drive inflammation and cancer when dysregulated.

Purpose of the Study:

  • To review the structure and function of well-defined NLR proteins.
  • To elucidate the association between NLRs and various human cancers.
  • To highlight the biological impact of NLRs in cancer development.

Main Methods:

  • Literature review of NLR protein structures and functions.
  • Analysis of signaling pathways downstream of NLR activation (inflammasomes, NF-κB, etc.).
  • Examination of evidence linking NLRs to pro-inflammatory conditions and cancer.

Main Results:

  • NLRs recognize pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs).
  • NLR signaling activates crucial immune pathways including inflammasomes and NF-κB.
  • Disruption of NLR signaling contributes to chronic inflammation and the development of human malignancies.

Conclusions:

  • NLR proteins are central regulators of innate immunity and inflammation.
  • Aberrant NLR function is implicated in the pathogenesis of diverse cancers.
  • Understanding NLRs offers potential therapeutic targets for cancer treatment.
Keywords:
NF-kBNLRNOD1NOD2cancerinflammasome

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