|
| 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
|
| 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.
|
| |
|
| 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
|
| |
|
| Contributor(s) |
Basak S, Banoth B |
| Citation(s) |
25905673 |
| |
| Submission date |
Oct 14, 2014 |
| Last update date |
Jun 14, 2018 |
| Contact name |
Balaji Banoth |
| E-mail(s) |
balajibanoth@nii.ac.in
|
| Organization name |
National Institute of Immunology
|
| Department |
Immunology
|
| Lab |
Systems Immunology Lab
|
| Street address |
Aruna Asaf Ali Marg
|
| City |
New Delhi |
| State/province |
Delhi |
| ZIP/Postal code |
110067 |
| Country |
India |
| |
|
| Platforms (1) |
| GPL6885 |
Illumina MouseRef-8 v2.0 expression beadchip |
|
| Samples (4)
|
|
| Relations |
| BioProject |
PRJNA263799 |