Activation of Innate Immunity in Graft-versus-Host Disease: Implications for Novel Targets?

被引:9
|
作者
Zeiser, Robert [1 ]
机构
[1] Univ Freiburg, Med Ctr, Dept Hematol & Oncol, D-79106 Freiburg, Germany
关键词
Graft-versus-host disease; Danger-associated molecular patterns; Innate immunity; Adenosine triphosphate; Uric acid; Purinergic receptors; Pattern recognition receptors; Syk; JAK1/2; RelB; STEM-CELL TRANSPLANTATION; T-CELLS; TYROSINE KINASE; DENDRITIC CELLS; INHIBITION; INFLAMMATION; BLOCKADE; GVHD; SYK; ATP;
D O I
10.1159/000381296
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Acute graft-versus-host disease (GvHD) is mediated by alloreactive donor-derived T cells with a suitable T cell receptor recognizing recipient major histocompatibility complex or minor histocompatibility antigens. However, the process of T cell activation and tissue injury sensing is also dependent on innate immune cells and non-hematopoietic cells. Different cell types of the innate immune system have the ability to sense danger-associated and pathogen-associated molecular patterns via pattern recognition receptors which can be transmembrane Toll-like receptors or cytoplasmic nucleotide-binding oligomerization domain-like receptors. Infectious stimuli include bacterial, viral, and fungal components, while non-infectious stimuli can be components derived from damaged cells or extracellular matrix. A better understanding of the complex sensing and effector mechanisms of innate immune cells in GvHD may help to improve preventive and therapeutic strategies in GvHD.
引用
收藏
页码:239 / 243
页数:7
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