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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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Related Experiment Video

Updated: Nov 2, 2025

Imaging Cell Membrane Injury and Subcellular Processes Involved in Repair
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ILC damage, and I'll repair it.

Chiara Sorini1, Eduardo J Villablanca1

  • 1Division of Immunology and Allergy, Department of Medicine Solna, Karolinska Institute and University Hospital Solna, 171 76 Stockholm, Sweden.

Immunity
|June 9, 2021
PubMed
Summary

Type 3 innate lymphoid cells sense cell damage through lysophosphatidyl serine and GPR43. This sensing triggers interleukin-22-dependent tissue repair mechanisms.

Area of Science:

  • Immunology
  • Cell Biology
  • Tissue Repair

Background:

  • Innate lymphoid cells (ILCs) are crucial for tissue homeostasis and immunity.
  • Type 3 ILCs (ILC3s) play a significant role in barrier immunity and tissue repair.
  • Mechanisms by which ILC3s sense tissue damage are not fully understood.

Purpose of the Study:

  • To investigate how type 3 innate lymphoid cells detect damage-induced cell death.
  • To identify the molecular pathways involved in ILC3 sensing of cellular damage.
  • To elucidate the role of ILC3s in initiating tissue repair following damage.

Main Methods:

  • Utilized mouse models of tissue injury.
  • Employed flow cytometry and gene expression analysis to study ILC3 function.

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  • Investigated the role of GPR43 and lysophosphatidyl serine in ILC3 activation.
  • Assessed the impact of ILC3 activation on interleukin-22 production and tissue repair.
  • Main Results:

    • Wang et al. demonstrate that GPR43 is expressed on type 3 innate lymphoid cells.
    • Lysophosphatidyl serine, a lipid released during cell death, is recognized by GPR43.
    • GPR43-mediated sensing of lysophosphatidyl serine activates ILC3s.
    • Activated ILC3s produce interleukin-22, promoting tissue repair.

    Conclusions:

    • Lysophosphatidyl serine recognition via GPR43 equips ILC3s to sense cell death.
    • This sensing mechanism triggers interleukin-22 production, driving essential tissue repair processes.
    • The findings reveal a novel pathway for innate immune cells to monitor tissue integrity and initiate repair.