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IL-33 in T Cell Differentiation, Function, and Immune Homeostasis

Michael Peine1, Roman M Marek2, Max Löhning1

  • 1Experimental Immunology and Osteoarthritis Research, Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany; Pitzer Laboratory of Osteoarthritis Research, German Rheumatism Research Center (DRFZ), Leibniz Institute, Charitéplatz 1, 10117 Berlin, Germany.

Trends in Immunology
|April 9, 2016
PubMed

Recent studies have highlighted a role for the alarmin interleukin (IL)-33 in CD4(+) and CD8(+) T cell activation and function, and have also revealed important distinctions. The IL-33 receptor ST2 is constitutively and abundantly expressed on T-helper-2 (Th2) and GATA-3(+) regulatory T cells in a GATA-3- and STAT5-dependent manner. Upon activation, Th1 and cytotoxic T cells express ST2 transiently, driven by T-bet and/or STAT4. We review these findings here, and critically examine evidence indicating that IL-33 enhances the differentiation and functionality of various T cell subsets through positive feedback loops involving lineage-specifying transcription factors. In this context, we discuss how quantitative and qualitative differences in ST2 expression between effector and GATA-3(+) regulatory T cells may contribute to immune homeostasis, and outline important areas of future inquiry.

Keywords:
CD4(+) and CD8(+) T cell subsetsST2/T1/IL-1RL1STAT4/STAT5T-bet/GATA-3/Foxp3Th1/Th2/Treg/CTLalarmin IL-33

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