PMID- 9034145
OWN - NLM
STAT- MEDLINE
DCOM- 19970314
LR  - 20231105
IS  - 0022-1007 (Print)
IS  - 1540-9538 (Electronic)
IS  - 0022-1007 (Linking)
VI  - 185
IP  - 4
DP  - 1997 Feb 17
TI  - IgE enhances mouse mast cell Fc(epsilon)RI expression in vitro and in vivo: 
      evidence for a novel amplification mechanism in IgE-dependent reactions.
PG  - 663-72
AB  - The binding of immunoglobulin E (IgE) to high affinity IgE receptors 
      (Fc(epsilon)RI) expressed on the surface of mast cells primes these cells to 
      secrete, upon subsequent exposure to specific antigen, a panel of proinflammatory 
      mediators, which includes cytokines that can also have immunoregulatory 
      activities. This IgE- and antigen-specific mast cell activation and mediator 
      production is thought to be critical to the pathogenesis of allergic disorders, 
      such as anaphylaxis and asthma, and also contributes to host defense against 
      parasites. We now report that exposure to IgE results in a striking (up to 
      32-fold) upregulation of surface expression of Fc(epsilon)RI on mouse mast cells 
      in vitro or in vivo. Moreover, baseline levels of Fc(epsilon)RI expression on 
      peritoneal mast cells from genetically IgE-deficient (IgE -/-) mice are 
      dramatically reduced (by approximately 83%) compared with those on cells from the 
      corresponding normal mice. In vitro studies indicate that the IgE-dependent 
      upregulation of mouse mast cell Fc(epsilon)RI expression has two components: an 
      early cycloheximide-insensitive phase, followed by a later and more sustained 
      component that is highly sensitive to inhibition by cycloheximide. In turn, 
      IgE-dependent upregulation of Fc(epsilon)RI expression significantly enhances the 
      ability of mouse mast cells to release serotonin, interleukin-6 (IL-6), and IL-4 
      in response to challenge with IgE and specific antigen. The demonstration that 
      IgE-dependent enhancement of mast cell Fc(epsilon)RI expression permits mast 
      cells to respond to antigen challenge with increased production of 
      proinflammatory and immunoregulatory mediators provides new insights into both 
      the pathogenesis of allergic diseases and the regulation of protective host 
      responses to parasites.
FAU - Yamaguchi, M
AU  - Yamaguchi M
AD  - Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical 
      School, Boston, Massachusetts 02215, USA.
FAU - Lantz, C S
AU  - Lantz CS
FAU - Oettgen, H C
AU  - Oettgen HC
FAU - Katona, I M
AU  - Katona IM
FAU - Fleming, T
AU  - Fleming T
FAU - Miyajima, I
AU  - Miyajima I
FAU - Kinet, J P
AU  - Kinet JP
FAU - Galli, S J
AU  - Galli SJ
LA  - eng
GR  - CA/AI-72074/CA/NCI NIH HHS/United States
GR  - R01 AI023990/AI/NIAID NIH HHS/United States
GR  - GM-53950/GM/NIGMS NIH HHS/United States
GR  - AI/CA-23990/AI/NIAID NIH HHS/United States
GR  - R37 GM053950/GM/NIGMS NIH HHS/United States
GR  - R37 AI023990/AI/NIAID NIH HHS/United States
GR  - R01 CA072074/CA/NCI NIH HHS/United States
GR  - R01 GM053950/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Exp Med
JT  - The Journal of experimental medicine
JID - 2985109R
RN  - 0 (Receptors, IgE)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 98600C0908 (Cycloheximide)
SB  - IM
MH  - Animals
MH  - Bone Marrow/drug effects/metabolism
MH  - Bone Marrow Cells
MH  - Cells, Cultured
MH  - Cycloheximide/pharmacology
MH  - Immunoglobulin E/*metabolism
MH  - Mast Cells/cytology/drug effects/*metabolism
MH  - Mice
MH  - Peritoneal Cavity/cytology
MH  - Receptors, IgE/*metabolism
MH  - Up-Regulation
PMC - PMC2196143
EDAT- 1997/02/17 00:00
MHDA- 1997/02/17 00:01
PMCR- 1997/08/17
CRDT- 1997/02/17 00:00
PHST- 1997/02/17 00:00 [pubmed]
PHST- 1997/02/17 00:01 [medline]
PHST- 1997/02/17 00:00 [entrez]
PHST- 1997/08/17 00:00 [pmc-release]
AID - 10.1084/jem.185.4.663 [doi]
PST - ppublish
SO  - J Exp Med. 1997 Feb 17;185(4):663-72. doi: 10.1084/jem.185.4.663.