PMID- 22868453
OWN - NLM
STAT- MEDLINE
DCOM- 20130527
LR  - 20180302
IS  - 1559-0488 (Electronic)
IS  - 1559-047X (Linking)
VI  - 33
IP  - 6
DP  - 2012 Nov-Dec
TI  - Dendritic cell depletion in burn patients is regulated by MafB expression.
PG  - 747-58
LID - 10.1097/BCR.0b013e318250457f [doi]
AB  - Studies have shown that monocytes are hyporesponsive and that dendritic cells 
      (DCs) are depleted in burn patients. We have recently shown in a mouse model that 
      burn injury alters the transcriptional regulation in bone marrow progenitors and 
      inhibits myeloid-derived DC (mDC) production. In the present study, using human 
      burn patient peripheral blood mononuclear cells, we have shown an overexpression 
      of MafB with a corresponding reduction in peripheral blood mononuclear 
      cell-derived mDCs. We isolated mononuclear cells from burn patient (23-68% TBSA) 
      and control volunteer peripheral blood samples by Ficoll gradient centrifugation 
      and cultured mDCs by using a standard ex vivo culture system. 
      Fluorescence-activated cell sorter analysis was used to select myeloid cells 
      based on the cell surface expression of CD45+. The mDC fraction was identified by 
      the expression of human leukocyte antigen (HLA)-DR+CD11c+, and we found a 
      significant reduction in HLA-DR+ leukocytes for up to 4 weeks postburn. MafB 
      expression was then examined in HLA-DR+CD14+ monocytes. Burn injury alters the 
      phenotype of CD14+ monocytes augmenting MafB expression and reducing their 
      differentiation into mDCs. MafB was then silenced in ex vivo culture prior to DC 
      differentiation by using small interfering RNA technique. MafB gene silencing 
      improved the differentiation potential of CD14+ cells into mDCs, increasing the 
      percentage of mDCs by >75%. Furthermore, GATA-1+ and HLA-DR+ mDCs were increased 
      following MafB silencing. Although burn injury augments the number of peripheral 
      blood monocytes, the frequency of mDC is reduced. This impairment is likely 
      secondary to the down-regulation of mDC differentiation by high MafB-expressing 
      monocytes following burn injury.
FAU - Williams, Keneeshia N
AU  - Williams KN
AD  - Department of Surgery, Loyola University Medical Center, Maywood, Illinois, USA.
FAU - Szilagyi, Andrea
AU  - Szilagyi A
FAU - He, Li-Ke
AU  - He LK
FAU - Conrad, Peggie
AU  - Conrad P
FAU - Halerz, Marcia
AU  - Halerz M
FAU - Gamelli, Richard L
AU  - Gamelli RL
FAU - Shankar, Ravi
AU  - Shankar R
FAU - Muthumalaiappan, Kuzhali
AU  - Muthumalaiappan K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Burn Care Res
JT  - Journal of burn care & research : official publication of the American Burn 
      Association
JID - 101262774
RN  - 0 (CD11c Antigen)
RN  - 0 (GATA1 Transcription Factor)
RN  - 0 (GATA1 protein, human)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 0 (MafB Transcription Factor)
RN  - 0 (RNA, Small Interfering)
RN  - EC 3.1.3.48 (Leukocyte Common Antigens)
RN  - EC 3.1.3.48 (PTPRC protein, human)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Analysis of Variance
MH  - Burns/*immunology/metabolism
MH  - CD11c Antigen/metabolism
MH  - Cells, Cultured
MH  - Dendritic Cells/*immunology
MH  - Female
MH  - Flow Cytometry
MH  - GATA1 Transcription Factor/metabolism
MH  - HLA-DR Antigens/metabolism
MH  - Humans
MH  - Leukocyte Common Antigens/metabolism
MH  - Lipopolysaccharide Receptors/metabolism
MH  - MafB Transcription Factor/*biosynthesis
MH  - Male
MH  - Microscopy, Confocal
MH  - Middle Aged
MH  - Monocytes/*immunology/metabolism
MH  - Phenotype
MH  - RNA, Small Interfering
EDAT- 2012/08/08 06:00
MHDA- 2013/05/29 06:00
CRDT- 2012/08/08 06:00
PHST- 2012/08/08 06:00 [entrez]
PHST- 2012/08/08 06:00 [pubmed]
PHST- 2013/05/29 06:00 [medline]
AID - 10.1097/BCR.0b013e318250457f [doi]
PST - ppublish
SO  - J Burn Care Res. 2012 Nov-Dec;33(6):747-58. doi: 10.1097/BCR.0b013e318250457f.