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Transcriptional analysis of the IL ‐33 receptor suppression of tumourigenicity 2 and its effects on canine Type 2 T helper cells: a preliminary study
Author(s) -
Asahina Ryota,
Nishida Hidetaka,
Kamishina Hiroaki,
Maeda Sadatoshi
Publication year - 2018
Publication title -
veterinary dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.744
H-Index - 60
eISSN - 1365-3164
pISSN - 0959-4493
DOI - 10.1111/vde.12512
Subject(s) - cytotoxic t cell , interleukin 33 , immunology , biology , transcription factor , interleukin , inflammation , receptor , t helper cell , microbiology and biotechnology , interleukin 12 , t cell , gene , cytokine , immune system , in vitro , genetics
Background Interleukin ( 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 ( ST 2), which is preferentially expressed on Th2 cells. The effects of IL ‐33 on canine Th2 cells are unclear. Hypothesis/Objectives ST 2 may be preferentially expressed on canine Th2 cells; IL ‐33 may induce the transcription of Th2 cytokines from these cells. Animals Three healthy dogs were used. Methods The transcription level of st2 was quantified in helper T cells, cytotoxic T cells and Th2 cells isolated from healthy dogs. The transcription levels of Th2 cytokines including il‐4 , il‐5 , il‐13 and il‐31 were quantified in Th2 cells stimulated with recombinant canine (rc) IL ‐33 and/or recombinant human (rh) IL ‐2. Results Transcription of st2 was the strongest in Th2 cells. Th2 cells also transcribed the genes for il‐5 and il‐13 after being stimulated with rc IL ‐33 and rh IL ‐2. Conclusions and clinical importance These results indicate that canine Th2 cells activated by IL ‐33 enhance Th2‐mediated inflammation through the production of IL ‐5 and IL ‐13.