PMID- 22539295
OWN - NLM
STAT- MEDLINE
DCOM- 20120706
LR  - 20211021
IS  - 1521-4141 (Electronic)
IS  - 0014-2980 (Print)
IS  - 0014-2980 (Linking)
VI  - 42
IP  - 5
DP  - 2012 May
TI  - Influence of hypoxia-inducible factor 1alpha on dendritic cell differentiation and 
      migration.
PG  - 1226-36
LID - 10.1002/eji.201142053 [doi]
AB  - Dendritic cells(DCs) are important sentinels of the immune system and frequently 
      reside in areas of low oxygen availability, in particular in the course of 
      inflammatory processes. Hypoxia-inducible transcription factor (HIF)1alpha is 
      responsible for major alterations in gene expression as part of the cellular 
      adaptation to low oxygen concentration. In this study, we generated mice with a 
      conditional deletion of HIF1alpha in DCs. Bone marrow-derived DCs from WT and 
      conditional mutant mice expressed elevated levels of major histocompatibility 
      complex class II and CD86 when grown in a hypoxic environment, whereas production 
      of the cytokines interleukin (IL)-12p70, IL-10, IL-6, TNF-alpha, IL-1beta, and IL-23 was 
      reduced, both independent of HIF1alpha expression. In contrast, secretion of IL-22 
      was strongly enhanced under hypoxic conditions in an HIF1alpha-dependent manner. The 
      chemokine receptor CCR7 was expressed at higher levels in wild-type DCs compared 
      with HIF1alpha-deficient DCs, whereas the production of CCL17 and CCL22 was increased 
      in conditions of low oxygen. Using in vitro as well as in vivo migration assays, 
      we observed an enhanced migratory capability of DCs generated under hypoxia, 
      which was HIF1alpha-dependent. Taken together, our data indicate that HIF1alpha plays an 
      important role for DC differentiation and migration in a low oxygen environment.
CI  - (c) 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
FAU - Kohler, Theresa
AU  - Kohler T
AD  - Molecular Immunology, IUF - Leibniz Research Institute for Environmental 
      Medicine, Dusseldorf, Germany.
FAU - Reizis, Boris
AU  - Reizis B
FAU - Johnson, Randall S
AU  - Johnson RS
FAU - Weighardt, Heike
AU  - Weighardt H
FAU - Forster, Irmgard
AU  - Forster I
LA  - eng
GR  - 092738/WT_/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Eur J Immunol
JT  - European journal of immunology
JID - 1273201
RN  - 0 (B7-2 Antigen)
RN  - 0 (Ccr7 protein, mouse)
RN  - 0 (Cd86 protein, mouse)
RN  - 0 (Cytokines)
RN  - 0 (Hif1a protein, mouse)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (Receptors, CCR7)
SB  - IM
MH  - Animals
MH  - B7-2 Antigen/biosynthesis/immunology
MH  - Bone Marrow Cells/immunology
MH  - Cell Differentiation/*immunology
MH  - Cell Hypoxia/immunology
MH  - Cell Movement/*immunology
MH  - Cells, Cultured
MH  - Cytokines/biosynthesis/immunology
MH  - Dendritic Cells/*immunology
MH  - Histocompatibility Antigens Class II/biosynthesis/immunology
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/biosynthesis/*immunology
MH  - Mice
MH  - Receptors, CCR7/biosynthesis/immunology
PMC - PMC6592818
MID - EMS83455
COIS- Conflict of interest: The authors declare no financial or commercial conflict of 
      interest.
EDAT- 2012/04/28 06:00
MHDA- 2012/07/07 06:00
PMCR- 2019/06/25
CRDT- 2012/04/28 06:00
PHST- 2012/04/28 06:00 [entrez]
PHST- 2012/04/28 06:00 [pubmed]
PHST- 2012/07/07 06:00 [medline]
PHST- 2019/06/25 00:00 [pmc-release]
AID - 10.1002/eji.201142053 [doi]
PST - ppublish
SO  - Eur J Immunol. 2012 May;42(5):1226-36. doi: 10.1002/eji.201142053.