Transcriptional analysis of the IL-33 receptor suppression of tumourigenicity 2 and its effects on canine Type 2 T helper cells: a preliminary study
Transcriptional analysis of the IL-33 receptor suppression of tumourigenicity 2 and its effects on canine Type 2 T helper cells: a preliminary study
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IL-33 受体抑制致瘤性 2 的转录分析及其对犬 2 型 T 辅助细胞的影响:初步研究
DOI:
10.1111/vde.12512
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发表时间:
2017
影响因子:
1.4
通讯作者:
Maeda Sadatoshi
中科院分区:
文献类型:
--
作者:
Asahina Ryota;Nishida Hidetaka;Kamishina Hiroaki;Maeda Sadatoshi
BackgroundInterleukin (IL)‐33 has been implicated in the pathogenesis of canine atopic dermatitis, a Type 2 T helper cell (Th2)‐associated disease. In humans, IL‐33 mediates its biological effects through the receptor suppression of tumourigenicity 2 (ST2), which is preferentially expressed on Th2 cells. The effects of IL‐33 on canine Th2 cells are unclear.Hypothesis/ObjectivesST2 may be preferentially expressed on canine Th2 cells; IL‐33 may induce the transcription of Th2 cytokines from these cells.AnimalsThree healthy dogs were used.MethodsThe transcription level ofst2was quantified in helper T cells, cytotoxic T cells and Th2 cells isolated from healthy dogs. The transcription levels of Th2 cytokines includingil‐4,il‐5,il‐13andil‐31were quantified in Th2 cells stimulated with recombinant canine (rc) IL‐33 and/or recombinant human (rh) IL‐2.ResultsTranscription ofst2was the strongest in Th2 cells. Th2 cells also transcribed the genes foril‐5andil‐13after being stimulated with rcIL‐33 and rhIL‐2.Conclusions and clinical importanceThese results indicate that canine Th2 cells activated by IL‐33 enhance Th2‐mediated inflammation through the production of IL‐5 and IL‐13.