PMID- 19779605
OWN - NLM
STAT- MEDLINE
DCOM- 20100201
LR  - 20231213
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 4
IP  - 9
DP  - 2009 Sep 25
TI  - SOCS2 influences LPS induced human monocyte-derived dendritic cell maturation.
PG  - e7178
LID - 10.1371/journal.pone.0007178 [doi]
LID - e7178
AB  - Dendritic cells (DCs) are highly specific antigen presenting cells, which link 
      innate and adaptive immune responses and participate in protecting hosts from 
      invading pathogens. DCs can be generated in vitro by culturing human monocytes 
      with GM-CSF and IL-4 followed by LPS induced DC maturation. We set out to study 
      the suppressor of cytokine signaling (SOCS) proteins during maturation and 
      activation of human monocyte-derived DCs from peripheral blood in vitro. We found 
      that the expression of SOCS2 mRNA and protein is dramatically up-regulated during 
      DC maturation. Silencing of SOCS2 using siRNA, inhibited DC maturation as 
      evidenced by a decreased expression of maturation markers such as CD83, 
      co-stimulatory molecules CD40, CD86 and HLA-DR. Furthermore, silencing of SOCS2 
      decreased LPS induced activation of MAP kinases (SAKP/JNK, p38, ERK), IRF3, 
      decreased the translocation of the NF-kappaB transcription factor and reduced 
      downstream gene mRNA expression. These results suggest a role for SOCS2 in the 
      MyD88-dependent and -independent TLR4 signaling pathways. In conclusion, our 
      results demonstrate that SOCS2 is required for appropriate TLR4 signaling in 
      maturating human DCs via both the MyD88-dependent and -independent signaling 
      pathway.
FAU - Hu, Jin
AU  - Hu J
AD  - Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, 
      Sweden.
FAU - Winqvist, Ola
AU  - Winqvist O
FAU - Flores-Morales, Amilcar
AU  - Flores-Morales A
FAU - Wikstrom, Ann-Charlotte
AU  - Wikstrom AC
FAU - Norstedt, Gunnar
AU  - Norstedt G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090925
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antigens, CD)
RN  - 0 (B7-2 Antigen)
RN  - 0 (CD40 Antigens)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (Immunoglobulins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (MYD88 protein, human)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (SOCS2 protein, human)
RN  - 0 (Suppressor of Cytokine Signaling Proteins)
RN  - 207137-56-2 (Interleukin-4)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Antigens, CD/biosynthesis
MH  - B7-2 Antigen/biosynthesis
MH  - CD40 Antigens/biosynthesis
MH  - Cells, Cultured
MH  - Dendritic Cells/*cytology
MH  - Gene Silencing
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/metabolism
MH  - HLA-DR Antigens/metabolism
MH  - Humans
MH  - Immunoglobulins/biosynthesis
MH  - Interleukin-4/metabolism
MH  - Lipopolysaccharides/*metabolism
MH  - Membrane Glycoproteins/biosynthesis
MH  - Monocytes/*cytology
MH  - Myeloid Differentiation Factor 88/metabolism
MH  - RNA, Small Interfering/metabolism
MH  - Suppressor of Cytokine Signaling Proteins/*metabolism/*physiology
MH  - CD83 Antigen
PMC - PMC2744869
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2009/09/26 06:00
MHDA- 2010/02/02 06:00
PMCR- 2009/09/25
CRDT- 2009/09/26 06:00
PHST- 2009/04/16 00:00 [received]
PHST- 2009/09/02 00:00 [accepted]
PHST- 2009/09/26 06:00 [entrez]
PHST- 2009/09/26 06:00 [pubmed]
PHST- 2010/02/02 06:00 [medline]
PHST- 2009/09/25 00:00 [pmc-release]
AID - 09-PONE-RA-09795R1 [pii]
AID - 10.1371/journal.pone.0007178 [doi]
PST - epublish
SO  - PLoS One. 2009 Sep 25;4(9):e7178. doi: 10.1371/journal.pone.0007178.