PMID- 12782712
OWN - NLM
STAT- MEDLINE
DCOM- 20030711
LR  - 20231103
IS  - 0022-1007 (Print)
IS  - 1540-9538 (Electronic)
IS  - 0022-1007 (Linking)
VI  - 197
IP  - 11
DP  - 2003 Jun 2
TI  - Preferential signaling and induction of allergy-promoting lymphokines upon weak 
      stimulation of the high affinity IgE receptor on mast cells.
PG  - 1453-65
AB  - Mast cell degranulation and de novo cytokine production is a consequence of 
      antigen-aggregation of the immunoglobulin E (IgE)-occupied high affinity receptor 
      for IgE (Fc epsilon RI). Herein, we report that lymphokines that promote allergic 
      inflammation, like MCP-1, were potently induced at low antigen (Ag) 
      concentrations or at low receptor occupancy with IgE whereas some that 
      down-regulate this response, like interleukin (IL)-10, required high receptor 
      occupancy. Weak stimulation of mast cells caused minimal degranulation whereas a 
      half-maximal secretory response was observed for chemokines and, with the 
      exception of TNF-alpha, a weaker cytokine secretory response was observed. The 
      medium from weakly stimulated mast cells elicited a monocyte/macrophage 
      chemotactic response similar to that observed at high receptor occupancy. Weak 
      stimulation also favored the phosphorylation of Gab2 and p38MAPK, while LAT and 
      ERK2 phosphorylation was induced by a stronger stimulus. Gab2-deficient mast 
      cells were severely impaired in chemokine mRNA induction whereas LAT-deficient 
      mast cells showed a more pronounced defect in cytokines. These findings 
      demonstrate that perturbation of small numbers of IgE receptors on mast cells 
      favors certain signals that contribute to a lymphokine response that can mediate 
      allergic inflammation.
FAU - Gonzalez-Espinosa, Claudia
AU  - Gonzalez-Espinosa C
AD  - Molecular Inflammation Section, Molecular Immunology and Inflammation Branch, 
      National Institute of Arthritis and Musculoskeletal and Skin Diseases, National 
      Institutes of Health, Bethesda, MD 20892, USA.
FAU - Odom, Sandra
AU  - Odom S
FAU - Olivera, Ana
AU  - Olivera A
FAU - Hobson, J Peyton
AU  - Hobson JP
FAU - Martinez, Maria Eugenia Cid
AU  - Martinez ME
FAU - Oliveira-Dos-Santos, Antonio
AU  - Oliveira-Dos-Santos A
FAU - Barra, Lillian
AU  - Barra L
FAU - Spiegel, Sarah
AU  - Spiegel S
FAU - Penninger, Josef M
AU  - Penninger JM
FAU - Rivera, Juan
AU  - Rivera J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
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 (Antigens)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Lymphokines)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, IgE)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Antigens/administration & dosage
MH  - Cell Degranulation/immunology
MH  - Chemokine CCL2/genetics
MH  - Chemokines/biosynthesis/genetics
MH  - Cytokines/biosynthesis/genetics
MH  - Female
MH  - Hypersensitivity/etiology/genetics/immunology
MH  - Immunoglobulin E/metabolism
MH  - In Vitro Techniques
MH  - Lymphokines/*biosynthesis/genetics
MH  - Male
MH  - Mast Cells/*immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mitogen-Activated Protein Kinase 1/metabolism
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Receptors, IgE/*metabolism
MH  - Signal Transduction
MH  - Tumor Necrosis Factor-alpha/genetics
MH  - p38 Mitogen-Activated Protein Kinases
PMC - PMC2193904
EDAT- 2003/06/05 05:00
MHDA- 2003/07/12 05:00
PMCR- 2003/12/02
CRDT- 2003/06/05 05:00
PHST- 2003/06/05 05:00 [pubmed]
PHST- 2003/07/12 05:00 [medline]
PHST- 2003/06/05 05:00 [entrez]
PHST- 2003/12/02 00:00 [pmc-release]
AID - jem.20021806 [pii]
AID - 20021806 [pii]
AID - 10.1084/jem.20021806 [doi]
PST - ppublish
SO  - J Exp Med. 2003 Jun 2;197(11):1453-65. doi: 10.1084/jem.20021806.