PMID- 23772226
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20130618
LR  - 20211021
IS  - 1664-3224 (Print)
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 4
DP  - 2013
TI  - The dendritic cell response to classic, emerging, and homeostatic danger signals. 
      Implications for autoimmunity.
PG  - 138
LID - 10.3389/fimmu.2013.00138 [doi]
LID - 138
AB  - Dendritic cells (DCs) initiate and control immune responses, participate in the 
      maintenance of immunological tolerance and are pivotal players in the 
      pathogenesis of autoimmunity. In patients with autoimmune disease and in 
      experimental animal models of autoimmunity, DCs show abnormalities in both 
      numbers and activation state, expressing immunogenic levels of costimulatory 
      molecules and pro-inflammatory cytokines. Exogenous and endogenous danger signals 
      activate DCs to stimulate the immune response. Classic endogenous danger signals 
      are released, activated, or secreted by host cells and tissues experiencing 
      stress, damage, and non-physiologic cell death; and are therefore referred to as 
      damage-associated molecular patterns (DAMPs). Some DAMPs are released from cells, 
      where they are normally sequestered, during necrosis (e.g., heat shock proteins, 
      uric acid, ATP, HMGB1, mitochondria-derived molecules). Others are actively 
      secreted, like Type I Interferons. Here we discuss important DAMPs in the context 
      of autoimmunity. For some, there is a clear pathogenic link (e.g., nucleic acids 
      and lupus). For others, there is less evidence. Additionally, we explore emerging 
      danger signals. These include inorganic materials and man-made technologies 
      (e.g., nanomaterials) developed as novel therapeutic approaches. Some 
      nanomaterials can activate DCs and may trigger unintended inflammatory responses. 
      Finally, we will review "homeostatic danger signals," danger signals that do not 
      derive directly from pathogens or dying cells but are associated with 
      perturbations of tissue/cell homeostasis and may signal pathological stress. 
      These signals, like acidosis, hypoxia, and changes in osmolarity, also play a 
      role in inflammation and autoimmunity.
FAU - Gallo, Paul M
AU  - Gallo PM
AD  - Laboratory of Dendritic Cell Biology, Department of Microbiology and Immunology, 
      Temple Autoimmunity Center, Temple University School of Medicine , Philadelphia, 
      PA , USA.
FAU - Gallucci, Stefania
AU  - Gallucci S
LA  - eng
PT  - Journal Article
DEP - 20130610
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
PMC - PMC3677085
OTO - NOTNLM
OT  - DAMPs
OT  - acidosis
OT  - autoimmunity
OT  - dendritic cells
OT  - hypoxia
OT  - mitochondria
OT  - nanomaterial
OT  - osmolarity
EDAT- 2013/06/19 06:00
MHDA- 2013/06/19 06:01
PMCR- 2013/01/01
CRDT- 2013/06/18 06:00
PHST- 2013/02/28 00:00 [received]
PHST- 2013/05/23 00:00 [accepted]
PHST- 2013/06/18 06:00 [entrez]
PHST- 2013/06/19 06:00 [pubmed]
PHST- 2013/06/19 06:01 [medline]
PHST- 2013/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2013.00138 [doi]
PST - epublish
SO  - Front Immunol. 2013 Jun 10;4:138. doi: 10.3389/fimmu.2013.00138. eCollection 
      2013.