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TLR3 signaling is downregulated by a MAVS isoform in epithelial cells

Omar Lakhdari1, Christopher S McAllister1, Michael Wang1

  • 1Laboratory of Mucosal Immunology, University of California San Diego, La Jolla, CA 92093, United States; Department of Medicine, University of California San Diego, La Jolla, CA 92093, United States.

Cellular Immunology
|September 6, 2016
PubMed

Insights

Mitochondrial antiviral signaling protein (MAVS) negatively regulates Toll-like receptor 3 (TLR3) signaling in epithelial cells. A specific MAVS isoform, miniMAVS, prevents excessive inflammatory responses to double-stranded RNA (dsRNA).

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Innate immune responses to double-stranded RNA (dsRNA) involve Toll-like receptor 3 (TLR3) and RIG-I-like receptor (RLR) pathways.
  • These pathways activate type I interferon (IFN), pro-inflammatory cytokines, and apoptosis.
  • The role of MAVS in TLR3-dependent responses to extracellular dsRNA remains unclear.

Purpose of the Study:

  • To investigate the role of MAVS in TLR3-dependent responses to extracellular dsRNA in epithelial cells.
  • To determine if MAVS isoforms regulate TLR3 signaling.

Main Methods:

  • Utilized a model of epithelial cells expressing a functional TLR3 signaling pathway.
  • Investigated the interaction between MAVS isoforms and TLR3 signaling.

Main Results:

  • TLR3-dependent responses to extracellular dsRNA were negatively regulated by MAVS.
  • A specific 50kDa isoform of MAVS, termed miniMAVS, was identified as the key regulator.
  • miniMAVS negatively regulates TLR3 signaling.

Conclusions:

  • MAVS, specifically the miniMAVS isoform, acts as an endogenous negative regulator of TLR3 signaling in epithelial cells.
  • This regulation by miniMAVS helps prevent excessive and potentially damaging inflammatory responses to extracellular dsRNA.
Keywords:
Epithelial cellsHCT116Interferon betaIsoformMAVSRegulationTLR3miniMAVS

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