TLR/MyD88-mediated Innate Immunity in Intestinal Graft-versus-Host Disease.
TLR/MyD88-mediated Innate Immunity in Intestinal Graft-versus-Host Disease.
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DOI：
10.4110/in.2017.17.3.144
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发表时间：
2017-06
期刊：
影响因子：
6
通讯作者：
Choi EY
中科院分区：
文献类型：
--
作者：
Lee YK;Kang M;Choi EY
移植物抗宿主病(GHVD)是异基因造血干细胞移植后的严重并发症。胃肠道是GVHD的主要靶器官，其炎症程度与疾病的严重程度相关。肠道炎症是由预适应照射引起的上皮损伤引起的。再加上供者来源的T细胞造成的损害，这种损害破坏了上皮屏障，使固有免疫细胞暴露在致病的和共生的肠道细菌面前，从而释放Toll样受体(TLRs)的配体。肠道微生物区系失调和TLR/髓系分化初级反应基因88(MyD88)信号通路参与了肠道移植物抗宿主病的发生。了解肠道GVHD中微生物区系的变化和TLR信号转导途径的作用，将有助于制定预防和治疗策略。
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.