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Journal article

CD45 exclusion and crosslinking-based receptor signaling together broaden FcεRI reactivity

Abstract:
For many years, the high-affinity receptor for immunoglobulin E (IgE) FcεRI, which is expressed by mast cells and basophils, has been widely held to be the exemplar of cross linking (that is, aggregation-dependent) signaling receptors. We found, however, that FcεRI signaling could occur in the presence or absence of receptor crosslinking. Using both cell and cell-free systems, we showed that FcεRI signaling was stimulated by surface-associated monovalent ligands through the passive, size-dependent exclusion of the receptor-type tyrosine phosphatase CD45 from plasma membrane regions of FcεRI-ligand engagement. Similarly to the T cell receptor, FcεRI signaling could also be initiated in a ligand-independent manner. These data suggest that a simple mechanism of CD45 exclusion–based receptor triggering could function together with crosslinking-based FcεRI signaling, broadening mast cell and basophil reactivity by enabling these cells to respond to both multivalent and surface-presented monovalent antigens. These findings also strengthen the case that a size-dependent, phosphatase exclusion– based receptor triggering mechanism might serve generally to facilitate signaling by noncatalytic immune receptors.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1126/scisignal.aat0756

Authors


More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
NDORMS
Sub department:
KIR
Role:
Author
More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
RDM
Sub department:
Weatherall Insti. of Molecular Medicine
Role:
Author
More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
RDM
Sub department:
Weatherall Insti. of Molecular Medicine
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Sub department:
Kennedy Institute for Rheumatology
Role:
Author
ORCID:
0000-0003-4983-6389


More from this funder
Funding agency for:
Felce, J
Dustin, M
Eggeling, C
Davis, S
Grant:
107375/Z/15/Z
100262/Z/12/Z
104924/14/Z/14
098274/Z/12/Z
091911


Publisher:
American Association for the Advancement of Science
Journal:
Science Signaling More from this journal
Volume:
11
Issue:
561
Pages:
eaat0756
Publication date:
2018-12-18
Acceptance date:
2018-11-30
DOI:
ISSN:
1937-9145 and 1945-0877


Pubs id:
pubs:949401
UUID:
uuid:2b046971-f83b-4700-83d1-be6df3808f0c
Local pid:
pubs:949401
Source identifiers:
949401
Deposit date:
2018-12-03

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