PMID- 28421078
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 1664-3224 (Print)
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 8
DP  - 2017
TI  - Genetic Association of Hematopoietic Stem Cell Transplantation Outcome beyond 
      Histocompatibility Genes.
PG  - 380
LID - 10.3389/fimmu.2017.00380 [doi]
LID - 380
AB  - The outcome of hematopoietic stem cell transplantation (HSCT) is controlled by 
      genetic factors among which the leukocyte antigen human leukocyte antigen (HLA) 
      matching is most important. In addition, minor histocompatibility antigens and 
      non-HLA gene polymorphisms in genes controlling immune responses are known to 
      contribute to the risks associated with HSCT. Besides single-nucleotide 
      polymorphisms (SNPs) in protein coding genes, SNPs in regulatory elements such as 
      microRNAs (miRNAs) contribute to these genetic risks. However, genetic risks 
      require for their realization the expression of the respective gene or miRNA. 
      Thus, gene and miRNA expression studies may help to identify genes and SNPs that 
      indeed affect the outcome of HSCT. In this review, we summarize gene expression 
      profiling studies that were performed in recent years in both patients and animal 
      models to identify genes regulated during HSCT. We discuss SNP-mRNA-miRNA 
      regulatory networks and their contribution to the risks associated with HSCT in 
      specific examples, including forkheadbox protein 3 and regulatory T cells, the 
      role of the miR-155 and miR-146a regulatory network for graft-versus-host 
      disease, and the function of MICA and its receptor NKG2D for the outcome of HSCT. 
      These examples demonstrate how SNPs affect expression or function of proteins 
      that modulate the alloimmune response and influence the outcome of HSCT. Specific 
      miRNAs targeting these genes and directly affecting expression of mRNAs are 
      identified. It might be valuable in the future to determine SNPs and to analyze 
      miRNA and mRNA expression in parallel in cohorts of HSCT patients to further 
      elucidate genetic risks of HSCT.
FAU - Gam, Rihab
AU  - Gam R
AD  - Hematological Sciences, Institute of Cellular Medicine, Newcastle University, 
      Newcastle upon Tyne, UK.
FAU - Shah, Pranali
AU  - Shah P
AD  - Institute of Cellular and Molecular Immunology, University Medical Centre 
      Gottingen, Gottingen, Germany.
FAU - Crossland, Rachel E
AU  - Crossland RE
AD  - Hematological Sciences, Institute of Cellular Medicine, Newcastle University, 
      Newcastle upon Tyne, UK.
FAU - Norden, Jean
AU  - Norden J
AD  - Hematological Sciences, Institute of Cellular Medicine, Newcastle University, 
      Newcastle upon Tyne, UK.
FAU - Dickinson, Anne M
AU  - Dickinson AM
AD  - Hematological Sciences, Institute of Cellular Medicine, Newcastle University, 
      Newcastle upon Tyne, UK.
FAU - Dressel, Ralf
AU  - Dressel R
AD  - Institute of Cellular and Molecular Immunology, University Medical Centre 
      Gottingen, Gottingen, Germany.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170403
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
PMC - PMC5377073
OTO - NOTNLM
OT  - MICA
OT  - forkheadbox protein 3
OT  - gene expression profiling
OT  - miR-146a
OT  - miR-155
OT  - microRNAs
OT  - non-human leukocyte antigen single-nucleotide polymorphisms
OT  - regulatory networks
EDAT- 2017/04/20 06:00
MHDA- 2017/04/20 06:01
PMCR- 2017/01/01
CRDT- 2017/04/20 06:00
PHST- 2016/08/03 00:00 [received]
PHST- 2017/03/16 00:00 [accepted]
PHST- 2017/04/20 06:00 [entrez]
PHST- 2017/04/20 06:00 [pubmed]
PHST- 2017/04/20 06:01 [medline]
PHST- 2017/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2017.00380 [doi]
PST - epublish
SO  - Front Immunol. 2017 Apr 3;8:380. doi: 10.3389/fimmu.2017.00380. eCollection 2017.