PMID- 15356155
OWN - NLM
STAT- MEDLINE
DCOM- 20041019
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 173
IP  - 6
DP  - 2004 Sep 15
TI  - Salmonella escape from antigen presentation can be overcome by targeting bacteria 
      to Fc gamma receptors on dendritic cells.
PG  - 4058-65
AB  - Dendritic cells (DCs) are professional APCs with the unique ability to activate 
      naive T cells, which is required for initiation of the adaptive immune response 
      against pathogens. Therefore, interfering with DC function would be advantageous 
      for pathogen survival and dissemination. In this study we provide evidence 
      suggesting that Salmonella enterica serovar typhimurium, the causative agent of 
      typhoid disease in the mouse, interferes with DC function. Our results indicate 
      that by avoiding lysosomal degradation, S. typhimurium impairs the ability of DCs 
      to present bacterial Ags on MHC class I and II molecules to T cells. This process 
      could correspond to a novel mechanism developed by this pathogen to evade 
      adaptive immunity. In contrast, when S. typhimurium is targeted to FcgammaRs on 
      DCs by coating bacteria with Salmonella-specific IgG, bacterial Ags are 
      efficiently processed and presented on MHC class I and class II molecules. This 
      enhanced Ag presentation leads to a robust activation of bacteria-specific T 
      cells. Laser confocal microscopy experiments show that virulent S. typhimurium is 
      rerouted to the lysosomal degradation pathway of DCs when internalized through 
      FcgammaR. These observations are supported by electron microscopy studies 
      demonstrating that internalized S. typhimurium shows degradation signs only when 
      coated with IgG and captured by FcgammaRs on DCs. Therefore, our data support a 
      potential role for bacteria-specific IgG on the augmentation of Ag processing and 
      presentation by DCs to T cells during the immune response against intracellular 
      bacteria.
CI  - Copyright 2004 The American Association of Immunologists, Inc.
FAU - Tobar, Jaime A
AU  - Tobar JA
AD  - Departamento de Genetica Molecular y Microbiologia, Facultad de Ciencias 
      Biologicas, Pontificia Universidad Catolica de Chile, Santiago, Chile.
FAU - Gonzalez, Pablo A
AU  - Gonzalez PA
FAU - Kalergis, Alexis M
AU  - Kalergis AM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Antigens, Bacterial)
RN  - 0 (Egg Proteins)
RN  - 0 (H-2 Antigens)
RN  - 0 (H-2Kb protein, mouse)
RN  - 0 (OVA-8)
RN  - 0 (Peptide Fragments)
RN  - 0 (Receptors, IgG)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Animals
MH  - Antigen Presentation/genetics/*immunology
MH  - Antigens, Bacterial/immunology/metabolism
MH  - Cell Line
MH  - Dendritic Cells/enzymology/*immunology/metabolism/*microbiology
MH  - Egg Proteins/genetics/immunology/metabolism
MH  - H-2 Antigens/genetics/immunology/metabolism
MH  - Lysosomes/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Ovalbumin/genetics/immunology/metabolism
MH  - Peptide Fragments
MH  - Phagocytosis/immunology
MH  - Plasmids
MH  - Receptors, IgG/*metabolism/physiology
MH  - Salmonella typhi/genetics/*immunology/*metabolism/pathogenicity
MH  - T-Lymphocytes/enzymology/immunology/metabolism
MH  - Virulence/genetics/immunology
EDAT- 2004/09/10 05:00
MHDA- 2004/10/20 09:00
CRDT- 2004/09/10 05:00
PHST- 2004/09/10 05:00 [pubmed]
PHST- 2004/10/20 09:00 [medline]
PHST- 2004/09/10 05:00 [entrez]
AID - 173/6/4058 [pii]
AID - 10.4049/jimmunol.173.6.4058 [doi]
PST - ppublish
SO  - J Immunol. 2004 Sep 15;173(6):4058-65. doi: 10.4049/jimmunol.173.6.4058.