PMID- 17498052
OWN - NLM
STAT- MEDLINE
DCOM- 20070716
LR  - 20210105
IS  - 0105-2896 (Print)
IS  - 0105-2896 (Linking)
VI  - 217
DP  - 2007 Jun
TI  - Differential release of mast cell mediators and the pathogenesis of inflammation.
PG  - 65-78
AB  - Mast cells are well known for their involvement in allergic and anaphylactic 
      reactions, during which immunoglobulin E (IgE) receptor (Fc epsilon RI) 
      aggregation leads to exocytosis of the content of secretory granules (1000 nm), 
      commonly known as degranulation, and secretion of multiple mediators. Recent 
      findings implicate mast cells also in inflammatory diseases, such as multiple 
      sclerosis, where mast cells appear to be intact by light microscopy. Mast cells 
      can be activated by bacterial or viral antigens, cytokines, growth factors, and 
      hormones, leading to differential release of distinct mediators without 
      degranulation. This process appears to involve de novo synthesis of mediators, 
      such as interleukin-6 and vascular endothelial growth factor, with release 
      through secretory vesicles (50 nm), similar to those in synaptic transmission. 
      Moreover, the signal transduction steps necessary for this process appear to be 
      largely distinct from those known in Fc epsilon RI-dependent degranulation. How 
      these differential mast cell responses are controlled is still unresolved. No 
      clinically available pharmacological agents can inhibit either degranulation or 
      mast cell mediator release. Understanding this process could help develop mast 
      cell inhibitors of selective mediator release with novel therapeutic 
      applications.
FAU - Theoharides, Theoharis C
AU  - Theoharides TC
AD  - Laboratory of Molecular Immunopharmacology and Drug Discovery, Department of 
      Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, 
      Tufts - New England Medical Center, Boston, MA, USA. 
      theoharis.theoharides@tufts.edu
FAU - Kempuraj, Duraisamy
AU  - Kempuraj D
FAU - Tagen, Michael
AU  - Tagen M
FAU - Conti, Pio
AU  - Conti P
FAU - Kalogeromitros, Dimitris
AU  - Kalogeromitros D
LA  - eng
GR  - DK42409/DK/NIDDK NIH HHS/United States
GR  - DK55681/DK/NIDDK NIH HHS/United States
GR  - AR47652/AR/NIAMS NIH HHS/United States
GR  - NS55681/NS/NINDS NIH HHS/United States
GR  - R01 AR047652/AR/NIAMS NIH HHS/United States
GR  - DK62861/DK/NIDDK NIH HHS/United States
GR  - NS38326/NS/NINDS NIH HHS/United States
GR  - DK44816/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Review
PL  - England
TA  - Immunol Rev
JT  - Immunological reviews
JID - 7702118
RN  - 0 (Biogenic Monoamines)
RN  - 0 (Enzymes)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Peptides)
SB  - IM
EIN - Immunol Rev. 2007 Oct;219:204
MH  - Biogenic Monoamines/metabolism
MH  - Enzymes/metabolism
MH  - Humans
MH  - Inflammation/*immunology
MH  - Inflammation Mediators/metabolism
MH  - Mast Cells/*immunology
MH  - Multiple Sclerosis/*immunology
MH  - Peptides/metabolism
RF  - 194
EDAT- 2007/05/15 09:00
MHDA- 2007/07/17 09:00
CRDT- 2007/05/15 09:00
PHST- 2007/05/15 09:00 [pubmed]
PHST- 2007/07/17 09:00 [medline]
PHST- 2007/05/15 09:00 [entrez]
AID - IMR519 [pii]
AID - 10.1111/j.1600-065X.2007.00519.x [doi]
PST - ppublish
SO  - Immunol Rev. 2007 Jun;217:65-78. doi: 10.1111/j.1600-065X.2007.00519.x.