PMID- 28774715
OWN - NLM
STAT- MEDLINE
DCOM- 20180205
LR  - 20180205
IS  - 1095-9157 (Electronic)
IS  - 0896-8411 (Linking)
VI  - 85
DP  - 2017 Dec
TI  - Dendritic cell recruitment and activation in autoimmunity.
PG  - 126-140
LID - S0896-8411(17)30502-4 [pii]
LID - 10.1016/j.jaut.2017.07.012 [doi]
AB  - Dendritic cells (DCs) are professional antigen presenting cells displaying the 
      unique capability to activate naive T cells. DCs react to pathogen encounter also 
      by the production of mediators of inflammation, including pro-inflammatory 
      cytokines. Because of this complex role, any imbalance in DC function reflects 
      into defective or exaggerated immune response and tissue damage. DCs comprise two 
      main subsets, namely conventional or classical DCs (cDCs), that are dedicated 
      antigen presenting cells, and plasmacytoid DCs (pDCs), that respond to nucleic 
      acids by releasing high amounts of type I interferons (IFNs). Since the formal 
      demonstration that DC can prime autoreactive naive T cells, a full body of 
      evidence has implicated DCs in virtually all manifestations of autoimmunity, 
      although their exact pathogenic role often remains poorly characterized. The 
      recent availability of progressively more refined strategies of constitutive and 
      inducible DC ablation is contributing in defining the precise role of DCs at 
      least in some autoimmune disease models. This review aims at critically 
      summarizing the current literature concerning selected aspects of DC biology 
      that, when altered, facilitate autoimmunity. These aspects include: i) mechanisms 
      of tissue entry and accumulation, ii) mechanisms of activation and iii) 
      orchestration of the immune balance by cytokine production. A special focus will 
      be on inappropriate DC activation by signals released by damaged tissues via 
      innate immune receptors, such as Toll-like receptors. These signals are 
      responsible, in pDCs, for exaggerated type I IFN production, the hallmark of a 
      set of apparently distant autoimmune conditions such as systemic lupus 
      erythematosus and type 1 diabetes; whereas in cDCs, they trigger DC rapid 
      maturation and Th1/Th17 cytokine secretion. Tissue-derived molecules also 
      contribute to further promote tissue damage and autoantigen spreading, possibly 
      through pDC-derived Granzyme B secretion. Finally, the therapeutic possibilities 
      based on DC targeting in human autoimmune diseases will be briefly summarized.
CI  - Copyright (c) 2017 Elsevier Ltd. All rights reserved.
FAU - Sozzani, Silvano
AU  - Sozzani S
AD  - Department of Molecular and Translational Medicine, University of Brescia, 
      Brescia, Italy; Humanitas Clinical and Research Institute, Rozzano-Milano, Italy. 
      Electronic address: silvano.sozzani@unibs.it.
FAU - Del Prete, Annalisa
AU  - Del Prete A
AD  - Department of Molecular and Translational Medicine, University of Brescia, 
      Brescia, Italy; Humanitas Clinical and Research Institute, Rozzano-Milano, Italy.
FAU - Bosisio, Daniela
AU  - Bosisio D
AD  - Department of Molecular and Translational Medicine, University of Brescia, 
      Brescia, Italy.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170801
PL  - England
TA  - J Autoimmun
JT  - Journal of autoimmunity
JID - 8812164
RN  - 0 (Cytokines)
SB  - IM
MH  - Animals
MH  - Autoimmune Diseases/immunology
MH  - Autoimmunity/*immunology
MH  - Cytokines/immunology
MH  - Dendritic Cells/*immunology
MH  - Humans
MH  - Immunity, Innate/immunology
EDAT- 2017/08/05 06:00
MHDA- 2018/02/06 06:00
CRDT- 2017/08/05 06:00
PHST- 2017/07/24 00:00 [received]
PHST- 2017/07/26 00:00 [accepted]
PHST- 2017/08/05 06:00 [pubmed]
PHST- 2018/02/06 06:00 [medline]
PHST- 2017/08/05 06:00 [entrez]
AID - S0896-8411(17)30502-4 [pii]
AID - 10.1016/j.jaut.2017.07.012 [doi]
PST - ppublish
SO  - J Autoimmun. 2017 Dec;85:126-140. doi: 10.1016/j.jaut.2017.07.012. Epub 2017 Aug 
      1.