PMID- 16061819
OWN - NLM
STAT- MEDLINE
DCOM- 20051205
LR  - 20181113
IS  - 0027-8424 (Print)
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Linking)
VI  - 102
IP  - 32
DP  - 2005 Aug 9
TI  - B7-DC cross-linking restores antigen uptake and augments antigen-presenting cell 
      function by matured dendritic cells.
PG  - 11438-43
AB  - Dendritic cells (DCs) are classified in two states: immature DCs (iDCs), which 
      perform sentinel functions, sampling for antigen and danger signals, and mature 
      DCs (mDCs), which exhibit enhanced antigen-presenting functions but are no longer 
      capable of acquiring antigen. We now describe DCs with a different activation 
      phenotype: cells having the strong antigen-presenting functions of mDCs and the 
      antigen-acquiring functions of iDCs. We have described an antibody that binds the 
      costimulatory molecule B7-DC and activates DCs. The resulting phenotype is 
      distinct from iDCs or mDCs matured by using Toll-like receptor (TLR) agonists. 
      Ability to take up antigen increases, while expression of B71/2 costimulatory and 
      MHC molecules remains unchanged. DCs matured with TLR agonists and then 
      superactivated through B7-DC exhibit a previously unrecognized phenotype. These 
      DCs recover the ability to take up antigen, which is normally lost after 
      treatment with TLR-3 and TLR-9 agonists, yet retain the high expression of 
      costimulatory and MHC molecules and strong antigen-presenting functions of mDCs. 
      Immunization using TLR agonists and B7-DC XAb (cross-linking antibody) together 
      as adjuvant resulted in substantially increased cytolytic T cell responses, 
      particularly when minimal peptide antigens were used. By stimulating DCs with two 
      distinct activation signals, a previously unrecognized phenotype exhibiting 
      augmented antigen-presenting functions was obtained.
FAU - Radhakrishnan, Suresh
AU  - Radhakrishnan S
AD  - Department of Immunology, Mayo Clinic College of Medicine, 200 First Street SW, 
      Rochester, MN 55905, USA.
FAU - Celis, Esteban
AU  - Celis E
FAU - Pease, Larry R
AU  - Pease LR
LA  - eng
GR  - R01 CA103921/CA/NCI NIH HHS/United States
GR  - R01CA80782/CA/NCI NIH HHS/United States
GR  - R01CA104996/CA/NCI NIH HHS/United States
GR  - R01CA103921/CA/NCI NIH HHS/United States
GR  - R01 CA096859/CA/NCI NIH HHS/United States
GR  - R01 CA080782/CA/NCI NIH HHS/United States
GR  - R01CA096859/CA/NCI NIH HHS/United States
GR  - R01 CA104996/CA/NCI NIH HHS/United States
GR  - P50CA91956/CA/NCI NIH HHS/United States
GR  - P50 CA091956/CA/NCI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Retracted Publication
DEP - 20050801
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (B7-1 Antigen)
RN  - 0 (Pdcd1lg2 protein, mouse)
RN  - 0 (Programmed Cell Death 1 Ligand 2 Protein)
SB  - IM
RIN - Radhakrishnan S, Celis E, Pease LR. Proc Natl Acad Sci U S A. 2010 May 
      4;107(18):8498. PMID: 20375280
MH  - Animals
MH  - Antibodies, Monoclonal/immunology
MH  - Antigen Presentation/*immunology
MH  - B7-1 Antigen/immunology/*metabolism
MH  - Cytotoxicity Tests, Immunologic
MH  - Dendritic Cells/*immunology/*metabolism
MH  - Flow Cytometry
MH  - *Immunization
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Programmed Cell Death 1 Ligand 2 Protein
PMC - PMC1183546
EDAT- 2005/08/03 09:00
MHDA- 2005/12/13 09:00
PMCR- 2006/02/09
CRDT- 2005/08/03 09:00
PHST- 2005/08/03 09:00 [pubmed]
PHST- 2005/12/13 09:00 [medline]
PHST- 2005/08/03 09:00 [entrez]
PHST- 2006/02/09 00:00 [pmc-release]
AID - 0501420102 [pii]
AID - 010211438 [pii]
AID - 10.1073/pnas.0501420102 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 2005 Aug 9;102(32):11438-43. doi: 
      10.1073/pnas.0501420102. Epub 2005 Aug 1.