PMID- 20030670
OWN - NLM
STAT- MEDLINE
DCOM- 20100816
LR  - 20211020
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Print)
IS  - 0009-9104 (Linking)
VI  - 160
IP  - 2
DP  - 2010 May
TI  - Dendritic cells pulsed with antigen-specific apoptotic bodies prevent 
      experimental type 1 diabetes.
PG  - 207-14
LID - 10.1111/j.1365-2249.2009.04082.x [doi]
AB  - Dendritic cells (DCs) are powerful antigen-presenting cells capable of 
      maintaining peripheral tolerance. The possibility to generate tolerogenic DCs 
      opens new therapeutic approaches in the prevention or remission of autoimmunity. 
      There is currently no treatment inducing long-term tolerance and remission in 
      type 1 diabetes (T1D), a disease caused by autoimmunity towards beta cells. An 
      ideal immunotherapy should inhibit the autoimmune attack, avoid systemic side 
      effects and allow islet regeneration. Apoptotic cells--a source of 
      autoantigens--are cleared rapidly by macrophages and DCs through an 
      immunologically silent process that contributes to maintaining tolerance. Our 
      aims were to prevent T1D and to evaluate the re-establishment of peripheral 
      tolerance using autologous DCs pulsed in vitro with apoptotic bodies from beta 
      cells. Immature DCs derived from bone marrow of non-obese diabetic (NOD) mice 
      were obtained and pulsed with antigen-specific apoptotic bodies from the beta 
      cell line NIT-1. Those DCs that phagocytosed apoptotic cells diminished the 
      expression of co-stimulatory molecules CD40 and CD86 and reduced secretion of 
      proinflammatory cytokines. Moreover, these cells were resistant to increase the 
      expression of co-stimulatory molecules after lipopolysaccharide activation. The 
      administration of these cells to NOD transgenic mice expressing interferon-beta 
      in their insulin-producing cells, a model of accelerated autoimmune diabetes, 
      decreased diabetes incidence significantly and correlated positively with 
      insulitis reduction. DCs pulsed with apoptotic cells that express 
      disease-associated antigens constitutes a promising strategy to prevent T1D.
FAU - Marin-Gallen, S
AU  - Marin-Gallen S
AD  - Laboratory of Immunobiology for Research and Diagnosis-Blood and Tissue Bank 
      (LIRAD-BST), Germans Trias i Pujol Research Institute, Department of Cellular 
      Biology, Physiology and Immunology, Autonomous University of Barcelona, 
      Barcelona, Spain.
FAU - Clemente-Casares, X
AU  - Clemente-Casares X
FAU - Planas, R
AU  - Planas R
FAU - Pujol-Autonell, I
AU  - Pujol-Autonell I
FAU - Carrascal, J
AU  - Carrascal J
FAU - Carrillo, J
AU  - Carrillo J
FAU - Ampudia, R
AU  - Ampudia R
FAU - Verdaguer, J
AU  - Verdaguer J
FAU - Pujol-Borrell, R
AU  - Pujol-Borrell R
FAU - Borras, F E
AU  - Borras FE
FAU - Vives-Pi, M
AU  - Vives-Pi M
LA  - eng
PT  - Evaluation Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20091217
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (Autoantigens)
RN  - 0 (Epitopes)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 77238-31-4 (Interferon-beta)
SB  - IM
MH  - Animals
MH  - Apoptosis/*immunology
MH  - Autoantigens/administration & dosage/*immunology
MH  - Cells, Cultured
MH  - Cytoplasmic Vesicles/immunology
MH  - *Dendritic Cells/immunology
MH  - Diabetes Mellitus, Type 1/genetics/immunology/*prevention & control
MH  - Endocytosis
MH  - Epitopes
MH  - Female
MH  - Immune Tolerance/*immunology
MH  - Immunotherapy/*methods
MH  - Insulin-Secreting Cells/*immunology/pathology
MH  - Interferon-beta/genetics
MH  - Lipopolysaccharides/pharmacology
MH  - Lymphocyte Activation/drug effects
MH  - Mice
MH  - Mice, Inbred NOD
MH  - Mice, Transgenic
MH  - Recombinant Fusion Proteins/genetics
MH  - Specific Pathogen-Free Organisms
PMC - PMC2857943
EDAT- 2009/12/25 06:00
MHDA- 2010/08/17 06:00
PMCR- 2011/05/01
CRDT- 2009/12/25 06:00
PHST- 2009/12/25 06:00 [entrez]
PHST- 2009/12/25 06:00 [pubmed]
PHST- 2010/08/17 06:00 [medline]
PHST- 2011/05/01 00:00 [pmc-release]
AID - CEI4082 [pii]
AID - 10.1111/j.1365-2249.2009.04082.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2010 May;160(2):207-14. doi: 10.1111/j.1365-2249.2009.04082.x. 
      Epub 2009 Dec 17.