PMID- 20124100
OWN - NLM
STAT- MEDLINE
DCOM- 20100504
LR  - 20211020
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 184
IP  - 5
DP  - 2010 Mar 1
TI  - Dendritic cell (DC)-specific targeting reveals Stat3 as a negative regulator of 
      DC function.
PG  - 2638-45
LID - 10.4049/jimmunol.0902960 [doi]
AB  - Dendritic cells (DCs) must achieve a critical balance between activation and 
      tolerance, a process influenced by cytokines and growth factors. IL-10, which 
      transduces signals through Stat3, has emerged as one important negative regulator 
      of DC activation. To directly examine the role Stat3 plays in regulating DC 
      activity, the Stat3 gene was targeted for deletion with a CD11c-cre transgene. 
      Stat3 CKO mice developed cervical lymphadenopathy as well as a mild ileocolitis 
      that persisted throughout life and was associated with impaired weight gain. 
      Consistent with this, Stat3-deficient DCs demonstrated enhanced immune activity, 
      including increased cytokine production, Ag-dependent T-cell activation and 
      resistance to IL-10-mediated suppression. These results reveal a cell-intrinsic 
      negative regulatory role of Stat3 in DCs and link increased DC activation with 
      perturbed immune homeostasis and chronic mucosal inflammation.
FAU - Melillo, Jessica A
AU  - Melillo JA
AD  - Department of Biological Sciences, Columbia University, New York, NY 10032, USA.
FAU - Song, Li
AU  - Song L
FAU - Bhagat, Govind
AU  - Bhagat G
FAU - Blazquez, Ana Belen
AU  - Blazquez AB
FAU - Plumlee, Courtney R
AU  - Plumlee CR
FAU - Lee, Carolyn
AU  - Lee C
FAU - Berin, Cecilia
AU  - Berin C
FAU - Reizis, Boris
AU  - Reizis B
FAU - Schindler, Christian
AU  - Schindler C
LA  - eng
GR  - T32 AI007525-09/AI/NIAID NIH HHS/United States
GR  - P01 AI050514-05/AI/NIAID NIH HHS/United States
GR  - P01 AI050514/AI/NIAID NIH HHS/United States
GR  - U19 AI044236/AI/NIAID NIH HHS/United States
GR  - HL 55413/HL/NHLBI NIH HHS/United States
GR  - AI 058211/AI/NIAID NIH HHS/United States
GR  - R01 AI058211-05S2/AI/NIAID NIH HHS/United States
GR  - 5T32 AI07525/AI/NIAID NIH HHS/United States
GR  - P01 AI044236/AI/NIAID NIH HHS/United States
GR  - R01 HL055413/HL/NHLBI NIH HHS/United States
GR  - R01 AI058211/AI/NIAID NIH HHS/United States
GR  - AI067804/AI/NIAID NIH HHS/United States
GR  - T32 AI007525/AI/NIAID NIH HHS/United States
GR  - R21 AI067804/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20100201
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (CD11c Antigen)
RN  - 0 (Cytokines)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - CD11c Antigen/genetics/metabolism
MH  - Cells, Cultured
MH  - Crohn Disease/genetics/metabolism/pathology
MH  - Cytokines/blood/metabolism
MH  - Dendritic Cells/drug effects/*immunology/*metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Flow Cytometry
MH  - Interferon-gamma/blood/metabolism
MH  - Interleukin-10/pharmacology
MH  - Lymphatic Diseases/genetics/metabolism/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Inbred Strains
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - STAT3 Transcription Factor/genetics/*metabolism
MH  - Tumor Necrosis Factor-alpha/blood/metabolism
PMC - PMC3099405
MID - NIHMS277314
COIS- Disclosures The authors have no financial conflicts of interest.
EDAT- 2010/02/04 06:00
MHDA- 2010/05/05 06:00
PMCR- 2011/05/23
CRDT- 2010/02/04 06:00
PHST- 2010/02/04 06:00 [entrez]
PHST- 2010/02/04 06:00 [pubmed]
PHST- 2010/05/05 06:00 [medline]
PHST- 2011/05/23 00:00 [pmc-release]
AID - jimmunol.0902960 [pii]
AID - 10.4049/jimmunol.0902960 [doi]
PST - ppublish
SO  - J Immunol. 2010 Mar 1;184(5):2638-45. doi: 10.4049/jimmunol.0902960. Epub 2010 
      Feb 1.