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Aggregated and Hyperstable Damage-Associated Molecular Patterns Are Released During ER Stress to Modulate Immune

Alexander Andersohn1, M Iveth Garcia1, Ying Fan1

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Frontiers in Cell and Developmental Biology
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Summary

Severe injury causes chronic endoplasmic reticulum (ER) stress, releasing stable damage-associated molecular patterns (DAMPs). These DAMPs activate immune cells, driving long-term systemic inflammation and poor outcomes.

Keywords:
DAMPER stressburncytokinedamage-associated molecular patterndendritic cellinflammationtrauma

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Area of Science:

  • Immunology
  • Cellular Biology
  • Stress Response

Background:

  • Chronic endoplasmic reticulum (ER) stress arises from unresolved protein misfolding, persisting despite the unfolded protein response.
  • Traumatic injuries, like severe burns, induce chronic ER stress and long-lasting systemic inflammation.
  • The mechanisms connecting chronic ER stress to sustained inflammation are not fully understood.

Purpose of the Study:

  • To investigate the link between chronic ER stress and systemic inflammation.
  • To identify molecules released during chronic ER stress that mediate inflammatory responses.
  • To understand how these molecules activate immune cells and influence T cell polarization.

Main Methods:

  • Induction of chronic ER stress in vivo following traumatic injury.
  • Analysis of secreted molecules, including known and novel damage-associated molecular patterns (DAMPs).
  • Assessment of DAMP aggregation, protease resistance, and their ability to activate dendritic cells (DCs) and polarize T cells.

Main Results:

  • Chronic ER stress leads to the release of aggregated and protease-resistant DAMPs.
  • These ER stress-derived DAMPs activate dendritic cells.
  • Activated DCs subsequently polarize naïve T cells, suggesting a role in adaptive immunity.

Conclusions:

  • Chronic ER stress releases hyperstable DAMPs into circulation.
  • These DAMPs contribute to persistent systemic inflammation after injury.
  • This mechanism may explain adverse outcomes associated with prolonged inflammation.