Constitutive overexpression of TNF in BPSM1 mice causes iBALT and bone marrow nodular lymphocytic hyperplasia

Seillet, Cyril; Carr, Elysa; Lacey, Derek; Stutz, Michael D.; Pellegrini, Marc; Whitehead, Lachlan; Rimes, Joel; Hawkins, Edwin D.; Roediger, Ben; Belz, Gabrielle T.; Bouillet, Philippe

doi:10.1111/imcb.12197

Cited by 2 publications

(2 citation statements)

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“…We have shown recently that, in addition to RA and heart valve disease, BPSM1 mice (both heterozygotes and homozygotes) also develop tertiary lymphoid organs (TLOs) such as inducible bronchus-associated lymphoid tissue (iBALT) and nodular lymphoid hyperplasia (NLH) in the bone marrow (5). Likewise, both TNFdel4 heterozygous and homozygous mice also developed iBALT and NLH ( Fig S1, and data not shown).…”

Section: Resultsmentioning

confidence: 84%

Severe dysregulation of TNF expression leads to multiple inflammatory diseases and embryonic death

Clayer

Dalseno

Kueh

et al. 2020

Preprint

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Post-transcriptional regulation mechanisms regulate mRNA stability or translational efficiency via ribosomes and recent evidence indicates that it is a major determinant of the accurate levels of cytokine mRNAs. While transcriptional regulation of Tnf has been well studied and found to be important for the rapid induction of Tnf mRNA and regulation of the acute phase of inflammation, study of its post-transcriptional regulation has been largely limited to the role of the AU-rich element (ARE), and to a lesser extent, that of the constitutive decay element (CDE). We have identified a new regulatory element (NRE) in the 3’ untranslated region (3’UTR) of Tnf, and demonstrate that ARE, CDE and NRE cooperate to efficiently down regulate Tnf expression and prevent autoimmune inflammatory diseases. We also show for the first time that excessive TNF may lead to embryonic death.

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Section: Resultsmentioning

confidence: 84%

Severe dysregulation of TNF expression leads to multiple inflammatory diseases and embryonic death

Clayer

Dalseno

Kueh

et al. 2020

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

“…We have shown recently that, in addition to RA and HVD, BPSM1 mice (both heterozygotes and homozygotes) also develop tertiary lymphoid organs such as inducible bronchus-associated lymphoid tissue (iBALT) and nodular lymphoid hyperplasia (NLH) in the bone marrow ( Seillet et al., 2019 ). Likewise, both TNFdel4 heterozygous and homozygous mice also developed iBALT and NLH ( Figure S2 , and data not shown).…”

Section: Resultsmentioning

confidence: 99%

Severe Impairment of TNF Post-transcriptional Regulation Leads to Embryonic Death

et al. 2020

Self Cite

View full text Add to dashboard Cite

Post-transcriptional regulation mechanisms control mRNA stability or translational efficiency via ribosomes, and recent evidence indicates that it is a major determinant of the accurate levels of cytokine mRNAs. Transcriptional regulation of Tnf has been well studied and found to be important for the rapid induction of Tnf mRNA and regulation of the acute phase of inflammation, whereas study of its post-transcriptional regulation has been largely limited to the role of the AU-rich element (ARE), and to a lesser extent, to that of the constitutive decay element (CDE). We have identified another regulatory element (NRE) in the 3 0 UTR of Tnf and demonstrate that ARE, CDE, and NRE cooperate in vivo to efficiently downregulate Tnf expression and prevent autoimmune inflammatory diseases. We also show that excessive TNF may lead to embryonic death.

show abstract

Constitutive overexpression of TNF in BPSM1 mice causes iBALT and bone marrow nodular lymphocytic hyperplasia

Cited by 2 publications

References 32 publications

Severe dysregulation of TNF expression leads to multiple inflammatory diseases and embryonic death

Severe dysregulation of TNF expression leads to multiple inflammatory diseases and embryonic death

Severe Impairment of TNF Post-transcriptional Regulation Leads to Embryonic Death

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