Next Article in Journal
De Novo Transcriptome Analysis of Differential Functional Gene Expression in Largemouth Bass (Micropterus salmoides) after Challenge with Nocardia seriolae
Previous Article in Journal
Parentage-Based Group Composition and Dispersal Pattern Studies of the Yangtze Finless Porpoise Population in Poyang Lake
Article Menu
Issue 8 (August) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2016, 17(8), 1288; doi:10.3390/ijms17081288

Role of Toll-Like Receptor Signaling in the Pathogenesis of Graft-versus-Host Diseases

1
Department of Haematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China
2
Second Clinical Medical College, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China
*
Author to whom correspondence should be addressed.
Academic Editors: Anthony Lemarié and Vera Sau-Fong Chan
Received: 6 April 2016 / Revised: 12 July 2016 / Accepted: 3 August 2016 / Published: 11 August 2016
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
View Full-Text   |   Download PDF [831 KB, uploaded 11 August 2016]   |  

Abstract

Graft-versus-host disease (GVHD) and infection are major complications after allogeneic hematopoietic stem cell transplantation (allo-HSCT) and the leading causes of morbidity and mortality in HSCT patients. Recent work has demonstrated that the two complications are interdependent. GVHD occurs when allo-reactive donor T lymphocytes are activated by major histocompatibility antigens or minor histocompatibility antigens on host antigen-presenting cells (APCs), with the eventual attack of recipient tissues or organs. Activation of APCs is important for the priming of GVHD and is mediated by innate immune signaling pathways. Current evidence indicates that intestinal microbes and innate pattern-recognition receptors (PRRs) on host APCs, including both Toll-like receptors (TLRs) and nucleotide oligomerization domain (NOD)-like receptors (NLRs), are involved in the pathogenesis of GVHD. Patients undergoing chemotherapy and/or total body irradiation before allo-HSCT are susceptible to aggravated gastrointestinal epithelial cell damage and the subsequent translocation of bacterial components, followed by the release of endogenous dangerous molecules, termed pathogen-associated molecular patterns (PAMPs), which then activate the PRRs on host APCs to trigger local or systemic inflammatory responses that modulate T cell allo-reactivity against host tissues, which is equivalent to GVHD. In other words, infection can, to some extent, accelerate the progression of GVHD. Therefore, the intestinal flora’s PAMPs can interact with TLRs to activate and mature APCs, subsequently activate donor T cells with the release of pro-inflammatory cytokines, and eventually, induce GVHD. In the present article, we summarize the current perspectives on the understanding of different TLR signaling pathways and their involvement in the occurrence of GVHD. View Full-Text
Keywords: TLRs; GVHD; PAMPs; HSCT TLRs; GVHD; PAMPs; HSCT
Figures

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Tu, S.; Zhong, D.; Xie, W.; Huang, W.; Jiang, Y.; Li, Y. Role of Toll-Like Receptor Signaling in the Pathogenesis of Graft-versus-Host Diseases. Int. J. Mol. Sci. 2016, 17, 1288.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top