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Status |
Public on May 01, 2015 |
Title |
Developmental LTbR synergistically activates TLR4 mediated inflammatory RelA/NF-kB response |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
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Summary |
Developmental signals are known to modulate inflammation. How ever, the mechanistic insight that links developmental and inflammatory signaling remains elusive. In the current study, we identifya critical role of NF-kB system in mediating stimulus specific crosstalk that allows developmental LTbR signals to sustain inflammatory TLR4 induced RelA/NF-kB response and gene expression. LTbR activated non-canonical signaling targets canonical TLR4 induced, nfkb2 encoded p100 not only to deplete inhibitory IkBd/(p100)2, but also to supplement RelA:p52/NF-kB dimers. Robust crosstalk in the gut epithelial cells are important, as crosstalk-defective nfkb2-/- mice succumbed to gut infection by Citrobacter rodentium due to hypo-inflammatory responses. Finally, we present evidence for a crosstalk motif that integrates tissue microenvironment derived developmental cues to ameliorate the pathogen response.
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Overall design |
Total RNA from WT early passage MEFs stimulated with ligands LPS, LTbR and LPS+LTbR for 24hrs were analyzed for global gene expression levels
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Contributor(s) |
Basak S, Banoth B |
Citation(s) |
25905673 |
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Submission date |
Oct 14, 2014 |
Last update date |
Jun 14, 2018 |
Contact name |
Balaji Banoth |
E-mail(s) |
balajibanoth@nii.ac.in
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Organization name |
National Institute of Immunology
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Department |
Immunology
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Lab |
Systems Immunology Lab
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Street address |
Aruna Asaf Ali Marg
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City |
New Delhi |
State/province |
Delhi |
ZIP/Postal code |
110067 |
Country |
India |
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Platforms (1) |
GPL6885 |
Illumina MouseRef-8 v2.0 expression beadchip |
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Samples (4)
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Relations |
BioProject |
PRJNA263799 |