Lee Young-Kwan, Kang Myungsoo, Choi Eun Young
Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
BioMembrane Plasticity Research Center (MPRC), Seoul National University College of Medicine, Seoul 03080, Korea.
Immune Netw. 2017 Jun;17(3):144-151. doi: 10.4110/in.2017.17.3.144. Epub 2017 Jun 20.
Graft-versus-host disease (GHVD) is a severe complication after allogeneic hematopoietic stem cell transplantation. The degree of inflammation in the gastrointestinal tract, a major GVHD target organ, correlates with the disease severity. Intestinal inflammation is initiated by epithelial damage caused by pre-conditioning irradiation. In combination with damages caused by donor-derived T cells, such damage disrupts the epithelial barrier and exposes innate immune cells to pathogenic and commensal intestinal bacteria, which release ligands for Toll-like receptors (TLRs). Dysbiosis of intestinal microbiota and signaling through the TLR/myeloid differentiation primary response gene 88 (MyD88) pathways contribute to the development of intestinal GVHD. Understanding the changes in the microbial flora and the roles of TLR signaling in intestinal GVHD will facilitate the development of preventative and therapeutic strategies.
移植物抗宿主病（GVHD）是异基因造血干细胞移植后的一种严重并发症。胃肠道作为主要的移植物抗宿主病靶器官，其炎症程度与疾病严重程度相关。肠道炎症由预处理放疗引起的上皮损伤引发。这种损伤与供体来源的T细胞造成的损伤共同作用，破坏上皮屏障，使天然免疫细胞暴露于致病性和共生性肠道细菌，这些细菌释放Toll样受体（TLR）的配体。肠道微生物群失调以及通过TLR/髓样分化初级反应基因88（MyD88）途径的信号传导促成了肠道移植物抗宿主病的发展。了解肠道微生物群的变化以及TLR信号在肠道移植物抗宿主病中的作用将有助于制定预防和治疗策略。
