The receptor-type protein tyrosine phosphatase CD45promotes onset and severity of IL-1 beta-mediated autoinflammatory osteomyelitis
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F21%3A10440407" target="_blank" >RIV/00216208:11310/21:10440407 - isvavai.cz</a>
Result on the web
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=gZ1Aipo5yF" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=gZ1Aipo5yF</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.jbc.2021.101131" target="_blank" >10.1016/j.jbc.2021.101131</a>
Alternative languages
Result language
angličtina
Original language name
The receptor-type protein tyrosine phosphatase CD45promotes onset and severity of IL-1 beta-mediated autoinflammatory osteomyelitis
Original language description
A number of human autoinflammatory diseases manifest withsevere inflammatory bone destruction. Mouse models of thesediseases represent valuable tools that help us to understand mo-lecular mechanisms triggering this bone autoinflammation. ThePstpip2cmomouse strain is among the best characterized of these;it harbors a mutation resulting in the loss of adaptor proteinPSTPIP2 and development of autoinflammatory osteomyelitis. InPstpip2cmomice, overproduction of interleukin-1 beta(IL-1 beta)andreactive oxygen species by neutrophil granulocytes leads tospontaneous inflammation of the bones and surrounding softtissues. However, the upstream signaling events leading to thisoverproduction are poorly characterized. Here, we show thatPstpip2cmomice deficient in major regulator of Src-family kinases(SFKs) receptor-type protein tyrosine phosphatase CD45 displaydelayed onset and lower severity of the disease, while the devel-opment of autoinflammation is not affected by deficiencies inToll-like receptor signaling. Our data also show deregulation ofpro-IL-1 beta production byPstpip2cmoneutrophils that are attenu-ated by CD45 deficiency. These data suggest a role for SFKs inautoinflammation. Together with previously published work onthe involvement of protein tyrosine kinase spleen tyrosine kinase,they point to the role of receptors containing immunoreceptortyrosine-based activation motifs, which after phosphorylation bySFKs recruit spleen tyrosine kinase for further signal propagation.We propose that this class of receptors triggers the eventsresulting in increased pro-IL-1 beta synthesis and disease initiationand/or progression.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30102 - Immunology
Result continuities
Project
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Continuities
S - Specificky vyzkum na vysokych skolach
Others
Publication year
2021
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Journal of Biological Chemistry [online]
ISSN
1083-351X
e-ISSN
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Volume of the periodical
297
Issue of the periodical within the volume
4
Country of publishing house
US - UNITED STATES
Number of pages
12
Pages from-to
101131
UT code for WoS article
000713100000010
EID of the result in the Scopus database
2-s2.0-85115411488