PMID- 22352313
OWN - NLM
STAT- MEDLINE
DCOM- 20120809
LR  - 20211021
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Print)
IS  - 0019-2805 (Linking)
VI  - 136
IP  - 3
DP  - 2012 Jul
TI  - IgG keeps virulent Salmonella from evading dendritic cell uptake.
PG  - 291-305
LID - 10.1111/j.1365-2567.2012.03578.x [doi]
AB  - Dendritic cells (DCs) are phagocytic professional antigen-presenting cells that 
      can prime naive T cells and initiate anti-bacterial immunity. However, several 
      pathogenic bacteria have developed virulence mechanisms to impair DC function. 
      For instance, Salmonella enterica serovar Typhimurium can prevent DCs from 
      activating antigen-specific T cells. In addition, it has been described that the 
      Salmonella Pathogenicity Island 1 (SPI-1), which promotes phagocytosis of 
      bacteria in non-phagocytic cells, can suppress this process in DCs in a 
      phosphatidylinositol 3-kinase (PI3K) -dependent manner. Both mechanisms allow 
      Salmonella to evade host adaptive immunity. Recent studies have shown that 
      IgG-opsonization of Salmonella can restore the capacity of DCs to present 
      antigenic peptide-MHC complexes and prime T cells. Interestingly, T-cell 
      activation requires Fcgamma receptor III (FcgammaRIII) expression over the DC surface, 
      suggesting that this receptor could counteract both antigen presentation and 
      phagocytosis evasion by bacteria. We show that, despite IgG-coated Salmonella 
      retaining its capacity to secrete anti-capture proteins, DCs are efficiently 
      capable of engulfing a large number of IgG-coated bacteria. These results suggest 
      that DCs employ another mechanism to engulf IgG-coated Salmonella, different from 
      that used for free bacteria. In this context, we noted that DCs do not employ 
      PI3K, actin cytoskeleton or dynamin to capture IgG-coated bacteria. Likewise, we 
      observed that the capture is an FcgammaR-independent mechanism. Interestingly, these 
      internalized bacteria were rapidly targeted for degradation within lysosomal 
      compartments. Hence, our results suggest a novel mechanism in DCs that does not 
      employ PI3K/actin cytoskeleton/dynamin/FcgammaRs to engulf IgG-coated Salmonella, is 
      not affected by anti-capture SPI-1-derived effectors and enhances DC 
      immunogenicity, bacterial degradation and antigen presentation.
CI  - (c) 2012 The Authors. Immunology (c) 2012 Blackwell Publishing Ltd.
FAU - Riquelme, Sebastian A
AU  - Riquelme SA
AD  - Millennium Institute of Immunology and Immunotherapy, Departamento de Genetica 
      Molecular y Microbiologia, Facultad de Ciencias Biologicas, Pontificia 
      Universidad Catolica de Chile Departamento de Reumatologia, Facultad de Medicina, 
      Pontificia Universidad Catolica de Chile, Santiago, Chile.
FAU - Bueno, Susan M
AU  - Bueno SM
FAU - Kalergis, Alexis M
AU  - Kalergis AM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Antigens, Bacterial)
RN  - 0 (Bacterial Proteins)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Opsonin Proteins)
RN  - 0 (Receptors, IgG)
RN  - 0 (Spi1 protein, Salmonella)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 3.6.5.5 (Dynamins)
SB  - IM
MH  - Actin Cytoskeleton/metabolism
MH  - Animals
MH  - Antigen Presentation
MH  - Antigens, Bacterial/metabolism
MH  - Bacterial Proteins/immunology
MH  - Dendritic Cells/*immunology/metabolism/*microbiology
MH  - Dynamins/metabolism
MH  - Immunoglobulin G/*metabolism
MH  - Lymphocyte Activation
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Opsonin Proteins/metabolism
MH  - Phagocytosis/immunology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Receptors, IgG/deficiency/genetics/metabolism
MH  - Salmonella typhimurium/*immunology/*pathogenicity
MH  - T-Lymphocytes/immunology
MH  - Virulence/immunology
PMC - PMC3385029
EDAT- 2012/02/23 06:00
MHDA- 2012/08/10 06:00
PMCR- 2013/07/01
CRDT- 2012/02/23 06:00
PHST- 2012/02/23 06:00 [entrez]
PHST- 2012/02/23 06:00 [pubmed]
PHST- 2012/08/10 06:00 [medline]
PHST- 2013/07/01 00:00 [pmc-release]
AID - 10.1111/j.1365-2567.2012.03578.x [doi]
PST - ppublish
SO  - Immunology. 2012 Jul;136(3):291-305. doi: 10.1111/j.1365-2567.2012.03578.x.