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. 2017 Apr 24;8:475. doi: 10.3389/fimmu.2017.00475

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Copyright © 2017 Griesenauer and Paczesny.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Pathogenesis of graft-versus-host disease (GVHD). The gut and other issues are damaged during irradiation or chemotherapy, leading to the release of various DAMPs, PAMPs, and cytokines, including IL-33. These DAMPs, PAMPs, and cytokines activate both host and donor antigen-presenting cells (APCs), which then activate the donor T cells. The APCs are also secreting various cytokines that promotes T cell differentiation toward type 1 and type 17 responses. These activated type 1 and type 17 T cells are able to secrete various pro-inflammatory cytokines, leading to apoptosis of healthy tissue, mainly in the gut, liver, and skin, which can be exacerbated by free IL-33. Furthermore, sST2 is produced by both type 1 and type 17 T cells, and while this may sequester free IL-33 from the type 1 and type 17 T cells, sST2 can also prevent the potential beneficial effects from ST2/IL-33 signaling in Th2 cells, Tregs, and lymphoid cell type 2 (ILC2s).