PMID- 20221401
OWN - NLM
STAT- MEDLINE
DCOM- 20110111
LR  - 20181113
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 5
IP  - 3
DP  - 2010 Mar 8
TI  - An NF-kappaB-dependent role for JunB in the induction of proinflammatory 
      cytokines in LPS-activated bone marrow-derived dendritic cells.
PG  - e9585
LID - 10.1371/journal.pone.0009585 [doi]
LID - e9585
AB  - BACKGROUND: Dendritic cells (DCs) play a key role in the induction of adaptive 
      and memory immune responses. Upon encounter with pathogens, they undergo a 
      complex maturation process and migrate toward lymphoid organs where they 
      stimulate immune effector cells. This process is associated with dramatic 
      transcriptome changes, pointing to a paramount role for transcription factors in 
      DC activation and function. The regulation and the role of these transcription 
      factors are however ill-defined and require characterization. Among those, AP-1 
      is a family of dimeric transcription complexes with an acknowledged role in the 
      control of immunity. However, it has not been studied in detail in DCs yet. 
      METHODOLOGY/PRINCIPAL FINDINGS: Here, we have investigated the regulation and 
      function of one of its essential components, JunB, in primary bone marrow-derived 
      DCs induced to maturate upon stimulation by Escherichia coli lipopolysaccharide 
      (LPS). Our data show fast and transient NF-kappaB-dependent transcriptional 
      induction of the junb gene correlating with the induction of the TNFalpha, IL-6, 
      and IL-12 proinflammatory cytokines. Inhibition of JunB protein induction by RNA 
      interference hampered the transcriptional activation of the TNF-alpha, IL-6, and 
      IL-12p40 genes. Consistently, chromatin immunoprecipitation experiments showed 
      LPS-inducible binding of JunB at AP-1-responsive sites found in promoter regions 
      of these genes. Concomitant LPS-inducible NF-kappaB/p65 binding to these 
      promoters was also observed. CONCLUSIONS/SIGNIFICANCE: We identified a novel role 
      for JunB--that is, induction of proinflammatory cytokines in LPS-activated 
      primary DCs with NF-kappaB acting not only as an inducer of JunB, but also as its 
      transcriptional partner.
FAU - Gomard, Tiphanie
AU  - Gomard T
AD  - Institut de Genetique Moleculaire de Montpellier, Centre National de la Recherche 
      Scientifique, Montpellier, France.
FAU - Michaud, Henri-Alexandre
AU  - Michaud HA
FAU - Tempe, Denis
AU  - Tempe D
FAU - Thiolon, Kevin
AU  - Thiolon K
FAU - Pelegrin, Mireia
AU  - Pelegrin M
FAU - Piechaczyk, Marc
AU  - Piechaczyk M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100308
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Chromatin)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Transcription Factor AP-1)
RN  - EC 2.7.11.10 (I-kappa B Kinase)
SB  - IM
MH  - Animals
MH  - Bone Marrow Cells/*cytology
MH  - Chromatin/metabolism
MH  - Dendritic Cells/*cytology
MH  - Escherichia coli/metabolism
MH  - Flow Cytometry/methods
MH  - Fluorescent Antibody Technique, Indirect
MH  - I-kappa B Kinase/metabolism
MH  - Inflammation
MH  - Lipopolysaccharides/*metabolism
MH  - Mice
MH  - NF-kappa B/*metabolism
MH  - Promoter Regions, Genetic
MH  - RNA, Small Interfering/metabolism
MH  - Transcription Factor AP-1/*metabolism
MH  - Transcriptional Activation
PMC - PMC2833204
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2010/03/12 06:00
MHDA- 2011/01/12 06:00
PMCR- 2010/03/08
CRDT- 2010/03/12 06:00
PHST- 2009/11/06 00:00 [received]
PHST- 2010/02/16 00:00 [accepted]
PHST- 2010/03/12 06:00 [entrez]
PHST- 2010/03/12 06:00 [pubmed]
PHST- 2011/01/12 06:00 [medline]
PHST- 2010/03/08 00:00 [pmc-release]
AID - 09-PONE-RA-14078R1 [pii]
AID - 10.1371/journal.pone.0009585 [doi]
PST - epublish
SO  - PLoS One. 2010 Mar 8;5(3):e9585. doi: 10.1371/journal.pone.0009585.