PMID- 11493612
OWN - NLM
STAT- MEDLINE
DCOM- 20010927
LR  - 20220330
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 70
IP  - 2
DP  - 2001 Aug
TI  - IgE-regulated loss, not IgE-regulated synthesis, controls expression of 
      FcepsilonRI in human basophils.
PG  - 207-18
AB  - Expression of the high-affinity receptor on basophils and mast cells is modulated 
      by immunoglobulin E (IgE) antibody. Recent studies have shown that modulation 
      occurs through interaction of IgE with the receptor itself, but the mechanisms 
      underlying this control are not understood. Taking both a theoretical and 
      experimental approach, we examined several competing models that focus on whether 
      there is IgE-regulated loss, IgE-regulated synthesis, or both regulated loss and 
      synthesis of the Fc receptor for IgE (FcepsilonRI). We report that removing IgE 
      from occupied FcepsilonRI resulted in an accelerated loss only in the unoccupied 
      receptor, with no loss of occupied receptors and no loss of total receptors when 
      all receptors were occupied. Together with previous studies, these results 
      establish that there was IgE-regulated loss of receptors. An examination of 
      synthetic rates of FcepsilonRIalpha using pulse-labeling with (35)S-methionine 
      indicated no difference in synthetic rates in the presence or absence of IgE. 
      Similarly, the presence or absence of IgE had no influence on the levels of mRNA 
      for either alpha, beta, or gamma subunits of FcepsilonRI. Using model 
      simulations, we found that regulated-synthesis models could be distinguished from 
      regulated-loss/constant-synthesis models on the basis of the relationship between 
      starting FcepsilonRI densities and changes in density after culture for 1 week in 
      the absence of IgE. Experimental data from this type of study fit a 
      regulated-loss model that did not include regulation of synthesis. Taken 
      together, these results suggest that IgE regulates cell surface expression of 
      FcepsilonRI only by regulating the rate that receptor is lost from the cell 
      surface.
FAU - MacGlashan, D Jr
AU  - MacGlashan D Jr
AD  - Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224, USA. 
      dmacglas@jhmi.edu
FAU - Xia, H Z
AU  - Xia HZ
FAU - Schwartz, L B
AU  - Schwartz LB
FAU - Gong, J
AU  - Gong J
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, IgE)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Basophils/*metabolism
MH  - Cells, Cultured
MH  - Computer Simulation
MH  - Humans
MH  - Immunoglobulin E/metabolism/*pharmacology
MH  - Inhibitory Concentration 50
MH  - Models, Biological
MH  - RNA, Messenger/drug effects/metabolism
MH  - Receptors, IgE/*biosynthesis/drug effects/genetics
MH  - Time Factors
MH  - Up-Regulation/drug effects
EDAT- 2001/08/09 10:00
MHDA- 2001/09/28 10:01
CRDT- 2001/08/09 10:00
PHST- 2001/08/09 10:00 [pubmed]
PHST- 2001/09/28 10:01 [medline]
PHST- 2001/08/09 10:00 [entrez]
PST - ppublish
SO  - J Leukoc Biol. 2001 Aug;70(2):207-18.