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The receptor-type protein tyrosine phosphatase CD45promotes onset and severity of IL-1 beta-mediated autoinflammatory osteomyelitis
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SYSNO ASEP 0554918 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title The receptor-type protein tyrosine phosphatase CD45promotes onset and severity of IL-1 beta-mediated autoinflammatory osteomyelitis Author(s) Králová, Jarmila (UMG-J)
Pavliuchenko, Nataliia (UMG-J)
Fabišik, Matěj (UMG-J)
Ilievová, Kristýna (UMG-J)
Špoutil, František (UMG-J)
Procházka, Jan (UMG-J) ORCID
Pokorná, Jana (UMG-J)
Sedláček, Radislav (UMG-J) RID
Brdička, Tomáš (UMG-J) RIDNumber of authors 9 Article number 101131 Source Title Journal of Biological Chemistry. - : Elsevier - ISSN 0021-9258
Roč. 297, č. 4 (2021)Number of pages 12 s. Publication form Online - E Language eng - English Country US - United States Keywords nlrp3 inflammasome ; signaling pathways ; kinase p50(csk) ; b-cell ; cd45 ; macrophages ; activation ; secretion ; mutation ; disease Subject RIV EB - Genetics ; Molecular Biology OECD category Developmental biology R&D Projects GA17-07155S GA ČR - Czech Science Foundation (CSF) GA19-05076S GA ČR - Czech Science Foundation (CSF) LM2018126 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) ED2.1.00/19.0395 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) ED1.1.00/02.0109 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) EF16_013/0001789 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) EF18_046/0015861 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) Research Infrastructure CCP II - 90126 - Ústav molekulární genetiky AV ČR, v. v. i. Method of publishing Open access Institutional support UMG-J - RVO:68378050 UT WOS 000713100000010 DOI 10.1016/j.jbc.2021.101131 Annotation 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. Workplace Institute of Molecular Genetics Contact Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Year of Publishing 2022 Electronic address https://linkinghub.elsevier.com/retrieve/pii/S0021925821009327
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