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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Apoptotic Cells Release IL1 Receptor Antagonist in Response to Genotoxic Stress

Jyh Yun Chwee1, Muznah Khatoo2, Nikki Yi Jie Tan2

  • 1Immunology Programme and Department of Microbiology and Immunology, Centre for Life Sciences, National University of Singapore, Singapore. National University of Singapore Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore.

Cancer Immunology Research
|February 14, 2016
PubMed

Insights

Apoptotic cells release interleukin-1 receptor antagonist (IL1RA), a key factor in suppressing inflammation. This release, dependent on DNA damage response and caspases, helps prevent inflammatory damage during programmed cell death.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Apoptosis is programmed cell death that normally prevents inflammation.
  • The mechanisms underlying the anti-inflammatory effects of apoptosis are not fully understood.

Purpose of the Study:

  • To investigate the molecular mechanisms by which apoptotic cells suppress inflammation.
  • To identify specific molecules released during apoptosis that mediate immunosuppression.

Main Methods:

  • Analysis of apoptotic cells induced by genotoxic stress.
  • Measurement of cytokine release using ELISA.
  • Western blotting to detect protein expression.
  • Caspase activity assays.

Main Results:

  • Apoptotic cells release interleukin-1 receptor antagonist (IL1RA).
  • IL1RA release is dependent on DNA damage response, caspase 9, and caspase 3.
  • IL1RA release does not require de novo translation, classical secretion, or N-glycosylation.
  • Released IL1RA inhibits IL1-induced IL6 expression.

Conclusions:

  • The release of IL1RA by apoptotic cells is a novel mechanism contributing to their immunosuppressive properties.
  • This pathway is crucial for preventing inflammatory responses and tissue damage following genotoxic stress.

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