Impact of GVHD on tissue regeneration and repair mechanisms. Tissue responses in steady state and/or the response to acute sterile injury (A, C, E) are compared with those observed during GVHD (B, D, F) for the intestine (A, B), thymus (C, D), and skin/lung (E, F). AhR, aryl hydrocarbon receptor; APC, antigen presenting cell; AREG, amphiregulin; BMP-4, bone morphogenetic protein 4; CM, corticomedullary; cTEC, cortical thymic epithelial cell; DAMP, damage-associated molecular pattern; DC, dendritic cell; DLL4, delta-like ligand 4; DP, double positive; EGF, epidermal growth factor; FcR, Fc receptor; FGF, fibroblast growth factor; GC, germinal center; GLP-2, glucagon-like peptide 2 (note was defined in text); Hsp47, heat shock protein 47; IFN-γ, interferon-γ; IGF-1, insulin-like growth factor 1; ILC, innate lymphoid cell; ISC, intestinal stem cell; KGF, keratinocyte growth factor; LEC, lymphatic endothelial cell; Mac, macrophage; mo, monocyte; mTEC, medullary thymic epithelial cell; PAMP, pathogen-associated molecular pattern; RANKL, receptor activator of NF-κΒ ligand; SP, single positive; Teff, effector T cell; TEPC, thymic epithelial progenitor cell; Tfh, follicular helper T cell; TGF-α/β, transforming growth factor-α/β; Th17, T helper 17 cell; Treg, regulatory T cell; VEGF, vascular endothelial growth factor; WNT, wingless-related integration site.