Reprint of: Acute Graft-versus-Host Disease: Novel Biological Insights

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Reprint of: Acute Graft-versus-Host Disease: Novel Biological Insights Takanori Teshima, Pavan Reddy, Robert Zeiser Biology of Blood and Marrow Transplantation Volume 22, Issue 3, Pages S3-S8 (March 2016) DOI: 10.1016/j.bbmt.2016.01.004 Copyright © 2016 Terms and Conditions

Figure 1 Homeostasis of self-renewing small intestinal epithelium results from ISCs, which locate at the base of the crypts and interspersed between their niche Paneth cells. IL-22 produced from innate lymphoid cells (ILCs) upon stimulation of IL-23 from antigen-presenting cells (APCs) and R-spondins play a role in self-renewal and differentiation of ISCs. Paneth cells maintain intestinal microbial ecology by secreting antimicrobial peptides (AMPs) into the lumen. Goblet cells shield the epithelium from luminal bacteria by secreting mucin. Intestinal homeostasis depends on proper interaction between the mucosal immune system and intestinal microbiota and its metabolites, such as butyrate. After allo-SCT, donor T cells and inflammatory cytokines, such as TNF, IL-6, and IL-1, damage the ISC-niche system. Paneth cell loss results in a reduced secretion of AMPs, leading to intestinal dysbiosis. Tissue injury permits translocation and dissemination of dominant luminal pathogens and pathogen-associated molecular patterns, which further accelerates GVHD by propagating a proinflammatory cytokine milieu. JAK-STAT pathways are required for responses to multiple cytokines and, thus, represent potential new targets in GVHD. Biology of Blood and Marrow Transplantation 2016 22, S3-S8DOI: (10.1016/j.bbmt.2016.01.004) Copyright © 2016 Terms and Conditions