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Innate immune memory: Implications for host responses to damage-associated molecular patterns.

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Innate immune cells can develop trained immunity, a form of epigenetic memory, in response to microbial or damage signals. This memory enhances inflammatory responses, offering new intervention possibilities for aging and autoinflammatory disorders.

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Damage-associated molecular patterns ⋅ Epigenetics ⋅ Innate immune memory ⋅Trained immunity

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Area of Science:

  • Immunology
  • Epigenetics
  • Cellular Biology

Background:

  • Innate immune cells acquire immunological memory through epigenetic reprogramming following stimulation.
  • This process, known as trained immunity, enhances inflammatory responses to subsequent challenges.
  • Previous studies focused on microbial ligands, but endogenous signals also induce similar reprogramming.

Purpose of the Study:

  • To review novel data on how endogenous damage-associated molecular patterns (DAMPs) induce trained immunity.
  • To highlight the role of epigenetic regulation in DAMP-induced trained immunity.
  • To explore the implications of DAMP-induced trained immunity in sterile inflammation and disease.

Main Methods:

  • Review of existing and novel scientific literature on trained immunity and DAMPs.
  • Analysis of epigenomic data from trained monocytes.
  • Discussion of transcriptional programs regulated by DAMPs.

Main Results:

  • Endogenous alarm signals (DAMPs) can induce trained immunity via epigenetic mechanisms.
  • DAMPs trigger long-term reprogramming of cytokine production and inflammatory responses.
  • Tissue-derived signals critically influence the host's immune response magnitude and type.

Conclusions:

  • DAMPs are potent inducers of trained immunity, contributing to persistent inflammation.
  • Understanding DAMP-induced trained immunity offers new therapeutic avenues for aging and autoinflammatory conditions.
  • Epigenetic reprogramming by DAMPs is a key mechanism in sterile inflammation.