Interplay of NLRC4/NLRP3 inflammasomes and Fc-ˠ-Receptors on CD1c+ DC Associates with Pathogenic IFNˠ+IL17+ T cells and RA Severity
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ABSTRACT:
PROVIDER: PRJNA659983 | ENA |
REPOSITORIES: ENA
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2018-04-27 | GSE110452 | GEO
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2014-09-08 | GSE57253 | GEO
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2012-01-01 | E-GEOD-34492 | biostudies-arrayexpress
Project description:Bacterial flagellin is a dominant innate immune activator of the intestine. Therefore, we examined the role of the intracellular flagellin receptor, NLRC4, in protecting the gut and/or driving inflammation. In accord with NLRC4 acting via transcription-independent pathways, loss of NLRC4 did not reduce the rapid robust changes in intestinal gene expression induced by flagellin administration. Loss of NLRC4 did not alter basal intestinal homeostasis nor predispose mice to development of colitis upon administration of an anti-IL-10R monoclonal antibody. However, in response to epithelial injury induced by dextran sulfate sodium (DSS), loss of NLRC4 resulted in more severe disease indicating a role for NLRC4 in protecting the gut. Moreover, loss of NLRC4 resulted in increased mortality in response to flagellate, but not aflagellate Salmonella infection. Thus, despite not being involved in rapid intestinal gene remodeling upon detection of flagellin, NLRC4-mediated inflammasome activation protects mice from mucosal and systemic challenges
2012-01-01 | GSE34492 | GEO
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2023-10-09 | GSE243588 | GEO
Project description:Purpose: Nlrc4-T337S mice have shown phenotypic differences in their intenstinal epithelia. The goal of this experiment was to determine the differences at the level of transcription between Nlrc4-T337S mice and WT in order to identify further areas of inquiry. Methods: Pooled cDNA libraries were sequenced on Illumina HiSeq 2000 platform, mapped to mm9 using Tophat v2.1, and quantified using Partek GSv6.6 software. Reads were converted to TPM and a 0.5 TPM offset added to all transcripts. Non-coding genes and genes with no sample > 1 TPM were removed Results: Using tophat/2.1.0, we mapped about 50 million sequence reads per sample to the mouse genome (build mm9) and identified 22986 transcripts in the intestines of WT and Nlrc4-T337S mice. Compared to WT IECs, Nlrc4-T337S had a 17-fold increase in Ubd, as well as increases in multiple genes that were identified as part of the MHC-II antigen presentation pathway. Conclusions: Our study found that Nlrc4-T337S IECs have a different RNA-profile than WT mice caused by their point mutation, which led to the discovery of increased proliferation of Nlrc4-T337S IECs as well as increased MHC-II expression.
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