PMID- 35203273
OWN - NLM
STAT- MEDLINE
DCOM- 20220408
LR  - 20220408
IS  - 2073-4409 (Electronic)
IS  - 2073-4409 (Linking)
VI  - 11
IP  - 4
DP  - 2022 Feb 11
TI  - FcepsilonRI: A Master Regulator of Mast Cell Functions.
LID - 10.3390/cells11040622 [doi]
LID - 622
AB  - Mast cells (MCs) perform multiple functions thought to underlie different 
      manifestations of allergies. Various aspects of antigens (Ags) and their 
      interactions with immunoglobulin E (IgE) cause diverse responses in MCs. FcepsilonRI, a 
      high-affinity IgE receptor, deciphers the Ag-IgE interaction and drives allergic 
      responses. FcepsilonRI clustering is essential for signal transduction and, therefore, 
      determines the quality of MC responses. Ag properties precisely regulate FcepsilonRI 
      dynamics, which consequently initiates differential outcomes by switching the 
      intracellular-signaling pathway, suggesting that Ag properties can control MC 
      responses, both qualitatively and quantitatively. Thus, the therapeutic benefits 
      of FcepsilonRI-targeting strategies have long been examined. Disrupting IgE-FcepsilonRI 
      interactions is a potential therapeutic strategy because the binding affinity 
      between IgE and FcepsilonRI is extremely high. Specifically, FcepsilonRI desensitization, due 
      to internalization, is also a potential therapeutic target that is involved in 
      the mechanisms of allergen-specific immunotherapy. Several recent findings have 
      suggested that silent internalization is strongly associated with FcepsilonRI dynamics. 
      A comprehensive understanding of the role of FcepsilonRI may lead to the development of 
      novel therapies for allergies. Here, we review the qualitatively diverse 
      responses of MCs that impact the attenuation/development of allergies with a 
      focus on the role of FcepsilonRI toward Ag exposure.
FAU - Nagata, Yuka
AU  - Nagata Y
AD  - Faculty of Pharmaceutical Science, Institute of Medical, Pharmaceutical and 
      Health Sciences, Kanazawa University, Kakuma-machi, Kanazawa 920-1192, Japan.
FAU - Suzuki, Ryo
AU  - Suzuki R
AUID- ORCID: 0000-0002-9580-7266
AD  - Faculty of Pharmaceutical Science, Institute of Medical, Pharmaceutical and 
      Health Sciences, Kanazawa University, Kakuma-machi, Kanazawa 920-1192, Japan.
LA  - eng
GR  - 20K15992 (to Y.N.) and 16H05082, 19H03369 (to R.S.)./Japan Society for the 
      Promotion of Science/
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20220211
PL  - Switzerland
TA  - Cells
JT  - Cells
JID - 101600052
RN  - 0 (Receptors, IgE)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Desensitization, Immunologic
MH  - Humans
MH  - *Hypersensitivity
MH  - Immunoglobulin E/metabolism
MH  - Mast Cells/metabolism
MH  - *Receptors, IgE/metabolism
PMC - PMC8870323
OTO - NOTNLM
OT  - FcepsilonRI
OT  - IgE
OT  - allergy
OT  - antigen
OT  - desensitization
OT  - mast cell
COIS- All the authors declare that they have no conflict of interest related to this 
      project.
EDAT- 2022/02/26 06:00
MHDA- 2022/04/09 06:00
PMCR- 2022/02/11
CRDT- 2022/02/25 01:01
PHST- 2021/12/30 00:00 [received]
PHST- 2022/01/29 00:00 [revised]
PHST- 2022/02/09 00:00 [accepted]
PHST- 2022/02/25 01:01 [entrez]
PHST- 2022/02/26 06:00 [pubmed]
PHST- 2022/04/09 06:00 [medline]
PHST- 2022/02/11 00:00 [pmc-release]
AID - cells11040622 [pii]
AID - cells-11-00622 [pii]
AID - 10.3390/cells11040622 [doi]
PST - epublish
SO  - Cells. 2022 Feb 11;11(4):622. doi: 10.3390/cells11040622.