The double-stranded RNA analogue polyinosinic-polycytidylic acid induces keratinocyte pyroptosis and release of IL-36γ.
The double-stranded RNA analogue polyinosinic-polycytidylic acid induces keratinocyte pyroptosis and release of IL-36γ.
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DOI：
10.1038/jid.2011.482
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发表时间：
2012-05
影响因子：
6.5
通讯作者：
Jensen, Liselotte E.
中科院分区：
文献类型：
--
作者：
Lian, Li-Hua;Milora, Katelynn A.;Manupipatpong, Katherine K.;Jensen, Liselotte E.
Interleukin-36 (IL-36) is the common name for the three IL-1 family members IL-36α, IL-36β and IL-36γ, formerly known as IL-1F6, IL-1F8 and IL-1F9, respectively. IL-36 appears to have pro-inflammatory activities; however, the physiological function of these cytokines remains unknown. Expression of IL-36 by keratinocytes implies its possible involvement in innate immune responses in the skin. We observed that, of the three IL-36 isoforms, human keratinocytes express high levels of IL-36γ. IL-36γ mRNA expression was dramatically induced by the Toll-like receptor ligands poly(I:C) and flagellin. Surprisingly, the IL-36γ protein was released by cells treated with poly(I:C) but remained intracellular in cells treated with flagellin only. Poly(I:C), but not flagellin, induced cell death and caspase-3/7 activation. Inhibition of caspase-3/7 and caspase-1 blocked extracellular release of IL-36γ from poly(I:C) treated cells. Furthermore, caspase-1 inhibition prevented poly(I:C)-induced caspase-3/7 activation. Interestingly, transcription of the gene IL36G was dependent upon caspase-1, but not caspase-3/7, activation. This demonstrates that the pathways leading to IL36G transcription and caspase-3/7 activation branch after caspase-1. This divergence of the pathways allows the cells to enter a state of de novo protein synthesis before committing to pyroptosis. Overall our observations suggest that IL-36γ may be an alarmin that signals the cause, e.g. viral infection, of cell death.
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DOI：
10.1165/rcmb.2009-0315oc
发表时间：
2011-02-01
影响因子：
6.4
作者：
Ramadas, Ravisankar A.;Ewart, Susan L.;LeVine, Ann Marie
通讯作者：
LeVine, Ann Marie
DOI：
10.4049/jimmunol.1003162
发表时间：
2011-02-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Johnston A;Xing X;Guzman AM;Riblett M;Loyd CM;Ward NL;Wohn C;Prens EP;Wang F;Maier LE;Kang S;Voorhees JJ;Elder JT;Gudjonsson JE
通讯作者：
Gudjonsson JE
影响因子：
4.4
作者：
Kalali, Behnam Naderi;Koellisch, Gabriele;Ollert, Markus
通讯作者：
Ollert, Markus
影响因子：
9.2
作者：
Feldmeyer, Laurence;Keller, Martin;Beer, Hans-Dietmar
通讯作者：
Beer, Hans-Dietmar
影响因子：
4.8
作者：
Kumar, S;McDonnell, PC;Young, PR
通讯作者：
Young, PR