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TLR/MyD88-mediated Innate Immunity in Intestinal Graft-versus-Host Disease
Immune Network ( IF 6 ) Pub Date : 2017-01-01 , DOI: 10.4110/in.2017.17.3.144
Young-Kwan Lee 1 , Myungsoo Kang 2 , Eun Young Choi 1, 2
Affiliation  

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.

中文翻译:

TLR/MyD88 介导的肠道移植物抗宿主病先天免疫

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(主要 GVHD 靶器官)的炎症程度与疾病严重程度相关。肠道炎症是由预处理辐射引起的上皮损伤引发的。与供体来源的 T 细胞造成的损伤相结合,这种损伤会破坏上皮屏障,并使先天免疫细胞暴露于致病性和共生肠道细菌,后者会释放 Toll 样受体 (TLR) 的配体。肠道微生物群的失调和通过 TLR/骨髓分化初级反应基因 88 (MyD88) 通路的信号传导有助于肠道 GVHD 的发展。
更新日期:2017-01-01
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