PMID- 26260212
OWN - NLM
STAT- MEDLINE
DCOM- 20160126
LR  - 20211203
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Linking)
VI  - 68
IP  - 2 Pt A
DP  - 2015 Dec
TI  - The role of dendritic cell alterations in susceptibility to hospital-acquired 
      infections during critical-illness related immunosuppression.
PG  - 120-3
LID - S0161-5890(15)30005-5 [pii]
LID - 10.1016/j.molimm.2015.06.030 [doi]
AB  - Systemic inflammatory response syndrome (SIRS) is a common condition in 
      critically ill patients. SIRS is characterized by alteration of both innate and 
      adaptive immunity and causes protracted immunosupression, exposing the patients 
      to severe secondary infections. Dendritic cells (DCs), which play a pivotal role 
      bridging innate and T cell-dependent immunity, exhibit prolonged alterations 
      after SIRS. In an early phase, SIRS causes depletion or systemic activation of 
      immature DCs in parenchymal tissues and lymphoid organs, leading to impaired 
      pathogen detection and presentation. Later on, newly formed DCs acquire a poorly 
      immunogenic phenotype, with poor capacity to capture, process and/or present 
      antigens and to stimulate T cells. Here, we review the studies that describe 
      alterations in DC function post-SIRS. Knowledge about the molecular mechanisms 
      involved are still scarce but their understanding might open new therapeutic 
      avenues to prevent or reduce protracted immunosuppression in critically-ill 
      patients.
CI  - Copyright (c) 2015 Elsevier Ltd. All rights reserved.
FAU - Roquilly, Antoine
AU  - Roquilly A
AD  - Department of Microbiology and Immunology, Doherty Institute of Infection and 
      Immunity, The University of Melbourne, Parkville, Victoria 3010, Australia.
FAU - Villadangos, Jose A
AU  - Villadangos JA
AD  - Department of Microbiology and Immunology, Doherty Institute of Infection and 
      Immunity, The University of Melbourne, Parkville, Victoria 3010, Australia; 
      Department of Biochemistry and Molecular Biology, Bio21 Molecular Science and 
      Biotechnology Institute, The University of Melbourne, Parkville, Victoria 3010, 
      Australia. Electronic address: j.villadangos@unimelb.edu.au.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20150808
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Antigens, Bacterial)
RN  - 0 (Antigens, Viral)
SB  - IM
MH  - *Antigen Presentation
MH  - Antigens, Bacterial/genetics/immunology
MH  - Antigens, Viral/genetics/immunology
MH  - Bacterial Infections/*immunology/microbiology/pathology
MH  - Critical Illness
MH  - Cross Infection/*immunology/microbiology/pathology/virology
MH  - Dendritic Cells/*immunology/metabolism/pathology
MH  - Disease Susceptibility
MH  - Humans
MH  - *Immunocompromised Host
MH  - Immunosuppression Therapy
MH  - Systemic Inflammatory Response 
      Syndrome/*immunology/microbiology/pathology/virology
MH  - T-Lymphocytes/immunology/pathology
MH  - Virus Diseases/immunology/pathology/virology
OTO - NOTNLM
OT  - Antigen-presentation
OT  - Critical-diseases
OT  - Dendritic cells
OT  - Infection
OT  - Systemic inflammation
EDAT- 2015/08/12 06:00
MHDA- 2016/01/27 06:00
CRDT- 2015/08/12 06:00
PHST- 2015/04/19 00:00 [received]
PHST- 2015/06/22 00:00 [revised]
PHST- 2015/06/24 00:00 [accepted]
PHST- 2015/08/12 06:00 [entrez]
PHST- 2015/08/12 06:00 [pubmed]
PHST- 2016/01/27 06:00 [medline]
AID - S0161-5890(15)30005-5 [pii]
AID - 10.1016/j.molimm.2015.06.030 [doi]
PST - ppublish
SO  - Mol Immunol. 2015 Dec;68(2 Pt A):120-3. doi: 10.1016/j.molimm.2015.06.030. Epub 
      2015 Aug 8.