PMID- 14657874
OWN - NLM
STAT- MEDLINE
DCOM- 20040123
LR  - 20220330
IS  - 0091-6749 (Print)
IS  - 0091-6749 (Linking)
VI  - 112
IP  - 6
DP  - 2003 Dec
TI  - Omalizumab treatment downregulates dendritic cell FcepsilonRI expression.
PG  - 1147-54
AB  - BACKGROUND: Dendritic cells (DCs) are potent antigen-presenting cells that 
      express FcepsilonRI, the high-affinity IgE receptor. Although the downregulation 
      of basophil FcepsilonRI during anti-IgE therapy with omalizumab is well 
      documented, its effect on FcepsilonRI expression by DCs has not been reported. 
      OBJECTIVE: We hypothesized that IgE regulates surface FcepsilonRI expression by 
      DCs in vivo and that, consequently, anti-IgE therapy decreases FcepsilonRI 
      expression by DCs. METHODS: In a randomized, double-blind, placebo-controlled 
      clinical trial 24 subjects (16 receiving omalizumab and 8 receiving placebo) with 
      seasonal allergic rhinitis received the study drug on days 0 and 28. Serial blood 
      samples drawn on days 0, 7, 14, 28, and 42 were analyzed for precursor DC1 (pDC1) 
      and pDC2 surface expression of FcepsilonRIalpha by using flow cytometry. RESULTS: 
      Omalizumab caused a significant decrease in surface FcepsilonRI expression at all 
      time points examined in both the pDC1 and pDC2 subsets. No significant change was 
      seen with placebo. The maximum decrease in FcepsilonRI expression in the 
      omalizumab group was 52% and 83%, respectively, for the pDC1 and pDC2 subsets. 
      The decrease in FcepsilonRI expression by both pDC subsets correlated with the 
      decrease in serum-free IgE and was of a similar magnitude to that found in 
      basophils. A 10-fold decrease in IgE corresponded to a 42% and 54% decrease in 
      surface FcepsilonRI expression by the pDC1 and pDC2 subsets, respectively. 
      CONCLUSION: These results demonstrate that anti-IgE therapy causes a rapid 
      decrease in DC surface FcepsilonRI expression and establish that IgE is an 
      important regulator of FcepsilonRI expression by DCs.
FAU - Prussin, Calman
AU  - Prussin C
AD  - Laboratory of Allergic Diseases, National Institute of Allergy and Infectious 
      Diseases, National Institutes of Health, Bethesda, MD, USA.
FAU - Griffith, Daniel T
AU  - Griffith DT
FAU - Boesel, Kevin M
AU  - Boesel KM
FAU - Lin, Henry
AU  - Lin H
FAU - Foster, Barbara
AU  - Foster B
FAU - Casale, Thomas B
AU  - Casale TB
LA  - eng
PT  - Clinical Trial
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Allergy Clin Immunol
JT  - The Journal of allergy and clinical immunology
JID - 1275002
RN  - 0 (Antibodies, Anti-Idiotypic)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Receptors, IgE)
RN  - 0 (anti-IgE antibodies)
RN  - 2P471X1Z11 (Omalizumab)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Adult
MH  - Ambrosia/adverse effects/immunology
MH  - Antibodies, Anti-Idiotypic/administration & dosage/therapeutic use
MH  - Antibodies, Monoclonal/administration & dosage/*therapeutic use
MH  - Antibodies, Monoclonal, Humanized
MH  - Dendritic Cells/immunology/*metabolism
MH  - Double-Blind Method
MH  - *Down-Regulation
MH  - Flow Cytometry
MH  - Humans
MH  - Immunoglobulin E/blood/immunology
MH  - Middle Aged
MH  - Omalizumab
MH  - Receptors, IgE/*metabolism
MH  - Rhinitis, Allergic, Seasonal/*drug therapy/etiology
MH  - Treatment Outcome
EDAT- 2003/12/06 05:00
MHDA- 2004/01/24 05:00
CRDT- 2003/12/06 05:00
PHST- 2003/12/06 05:00 [pubmed]
PHST- 2004/01/24 05:00 [medline]
PHST- 2003/12/06 05:00 [entrez]
AID - S0091674903024394 [pii]
AID - 10.1016/j.jaci.2003.10.003 [doi]
PST - ppublish
SO  - J Allergy Clin Immunol. 2003 Dec;112(6):1147-54. doi: 10.1016/j.jaci.2003.10.003.