title: Apoptotic Cells Release IL1 Receptor Antagonist in Response to Genotoxic Stress.
abstract: Apoptosis is a controlled means of eliminating damaged cells without causing an inflammatory response or tissue damage. The mechanisms that contribute to the suppression of an inflammatory response upon apoptosis of cells are poorly understood. Here, we report that apoptotic cells release the interleukin-1 receptor antagonist (IL1RA). The release of IL1RA depended on the DNA damage response, caspase 9, and caspase 3.De novotranslation, classical secretion pathways, or N-glycosylation was not required for the release of IL1RA. The amounts of IL1RA released by apoptotic cells impaired IL1-induced expression of IL6 In summary, we demonstrate that the release of IL1RA in response to genotoxic stress contributes to the immunosuppressive effects of apoptotic cells.
authors.affiliation: Immunology 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.
authors.forename: Jyh Yun
authors.initials: JY
authors.lastname: Chwee
authors.affiliation: Immunology Programme and Department of Microbiology and Immunology, Centre for Life Sciences, National University of Singapore, Singapore.
authors.forename: Muznah
authors.initials: M
authors.lastname: Khatoo
authors.affiliation: Immunology Programme and Department of Microbiology and Immunology, Centre for Life Sciences, National University of Singapore, Singapore.
authors.forename: Nikki Yi Jie
authors.initials: NY
authors.lastname: Tan
authors.affiliation: Immunology 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. micsg@nus.edu.sg.
authors.forename: Stephan
authors.initials: S
authors.lastname: Gasser
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics* / Q000276:immunology; D001761:Bleomycin / Q000494:pharmacology; D020169:Caspases / Q000378:metabolism; D002460:Cell Line; D004249:DNA Damage; D005347:Fibroblasts; D015870:Gene Expression; D006801:Humans; D056747:Immunomodulation; D053590:Interleukin 1 Receptor Antagonist Protein / Q000235:genetics / Q000378:metabolism*; D007375:Interleukin-1 / Q000378:metabolism; D008264:Macrophages; D051379:Mice; D014176:Protein Biosynthesis; D015398:Signal Transduction
chemical_list: D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D001761:Bleomycin; D020169:Caspases