PMID- 25204675
OWN - NLM
STAT- MEDLINE
DCOM- 20151026
LR  - 20231213
IS  - 1935-3456 (Electronic)
IS  - 1933-0219 (Print)
IS  - 1933-0219 (Linking)
VI  - 8
IP  - 2
DP  - 2015 Mar
TI  - Dendritic cell CD83 homotypic interactions regulate inflammation and promote 
      mucosal homeostasis.
PG  - 414-28
LID - 10.1038/mi.2014.79 [doi]
AB  - Dendritic cells (DCs) form an extensive network in the intestinal lamina propria, 
      which orchestrates the mucosal immune response. Alterations in DC function can 
      predispose to inflammatory bowel disease, although by unknown mechanisms. We show 
      that CD83, a highly regulated DC cell surface protein, modulates the immune 
      response to prevent colitis. Mice with a conditional knockout of CD83 in DCs 
      develop exacerbated colitis following dextran sodium sulfate challenge, whereas 
      mucosal overexpression of CD83 inhibits DC inflammatory response and protects 
      against colitis. These CD83 perturbations can be modeled in vitro where we show 
      that CD83 homotypic interaction occurs via cell-cell contact and inhibits 
      pro-inflammatory responses. CD83 knockdown or cytoplasmic truncation abrogates 
      the effects of homotypic binding. We demonstrate that CD83 homotypic interaction 
      regulates DC activation via the mitogen-activated protein kinase pathway by 
      inhibiting p38alpha phosphorylation. Our findings indicate that CD83 homotypic 
      interactions regulate DC activation and promote mucosal homeostasis.
FAU - Bates, J M
AU  - Bates JM
AD  - Department of Pathology, Genetech, South San Francisco, California, USA.
FAU - Flanagan, K
AU  - Flanagan K
AD  - Department of Pathology, Genetech, South San Francisco, California, USA.
FAU - Mo, L
AU  - Mo L
AD  - Department of Pathology, Genetech, South San Francisco, California, USA.
FAU - Ota, N
AU  - Ota N
AD  - Department of Immunology, Genetech, South San Francisco, California, USA.
FAU - Ding, J
AU  - Ding J
AD  - Department of Immunology, Genetech, South San Francisco, California, USA.
FAU - Ho, S
AU  - Ho S
AD  - Department of Pathology, Genetech, South San Francisco, California, USA.
FAU - Liu, S
AU  - Liu S
AD  - Department of Pathology, Genetech, South San Francisco, California, USA.
FAU - Roose-Girma, M
AU  - Roose-Girma M
AD  - Department of Molecular Biology, Genentech, South San Francisco, California, USA.
FAU - Warming, S
AU  - Warming S
AD  - Department of Molecular Biology, Genentech, South San Francisco, California, USA.
FAU - Diehl, L
AU  - Diehl L
AD  - Department of Pathology, Genetech, South San Francisco, California, USA.
LA  - eng
PT  - Journal Article
DEP - 20140910
PL  - United States
TA  - Mucosal Immunol
JT  - Mucosal immunology
JID - 101299742
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Surface)
RN  - 0 (Immunoglobulins)
RN  - 0 (Membrane Glycoproteins)
SB  - IM
MH  - Animals
MH  - Antigens, CD/genetics/*metabolism
MH  - Antigens, Surface/genetics/metabolism
MH  - Cell Communication
MH  - Colitis/genetics/immunology/metabolism/microbiology/pathology
MH  - Dendritic Cells/*immunology/*metabolism
MH  - Disease Models, Animal
MH  - Female
MH  - Gene Expression
MH  - *Homeostasis
MH  - Immunity, Mucosal
MH  - Immunoglobulins/genetics/*metabolism
MH  - Immunophenotyping
MH  - Inflammation/genetics/*immunology/*metabolism/pathology
MH  - Intestinal Mucosa/*immunology/*metabolism/microbiology/pathology
MH  - MAP Kinase Signaling System
MH  - Membrane Glycoproteins/genetics/*metabolism
MH  - Mice
MH  - Mice, Knockout
MH  - Protein Binding
MH  - Signal Transduction
MH  - CD83 Antigen
PMC - PMC4326976
EDAT- 2014/09/11 06:00
MHDA- 2015/10/27 06:00
PMCR- 2015/02/13
CRDT- 2014/09/11 06:00
PHST- 2013/09/24 00:00 [received]
PHST- 2014/07/26 00:00 [accepted]
PHST- 2014/09/11 06:00 [entrez]
PHST- 2014/09/11 06:00 [pubmed]
PHST- 2015/10/27 06:00 [medline]
PHST- 2015/02/13 00:00 [pmc-release]
AID - S1933-0219(22)00836-4 [pii]
AID - 10.1038/mi.2014.79 [doi]
PST - ppublish
SO  - Mucosal Immunol. 2015 Mar;8(2):414-28. doi: 10.1038/mi.2014.79. Epub 2014 Sep 10.