Event Abstract

Transcriptional regulation of the anti-inflammatory NLRP12/Monarch-1 by NF-kB

  • 1 Sapienza University of Rome, Italy

NLRP12 (NLR family, pyrin domain containing 12) is a NLR (Nucleotide-binding domain and leucine-rich repeat containing) protein which is expressed predominantly in cells of myeloid origin. It has been described as a negative regulator of both canonical and non-canonical NF-kB activation. Accordingly with its inhibitory function, NLRP12 expression is down-regulated following activation by TLR agonists or exposure of cells to inflammatory cytokines, whereas the expression of most NLR proteins is typically induced. It is hypothesized that the downregulation of NLRP12 expression is necessary for an appropriate immune response. After the removal of inflammatory stimuli, the expression level of NLRP12 should be restored to prevent excessive inflammation. To test this hypothesis, we focused on the control of NLRP12 expression at the transcriptional level. We asked if a NF-kB-driven, negative feedback mechanism causes the down-regulation of NLRP12 transcription. We will show our recent findings about the modulatory effects of NF-kB on the NLRP12 promoter. Moreover, work is in progress to analyze the modulation of NLRP12 protein expression during inflammation and differentiation of myeloid cells.

Keywords: NLRP12, NF-kB, Transcriptional regulation, differentiation, Inflammation

Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013.

Presentation Type: Abstract

Topic: Innate immunity

Citation: Tuncer S, Camperio C, Camilli G, Porciello N, Piccolella E, Fiorillo M and Sorrentino R (2013). Transcriptional regulation of the anti-inflammatory NLRP12/Monarch-1 by NF-kB. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00127

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Received: 11 Mar 2013; Published Online: 22 Aug 2013.

* Correspondence: Mrs. Sinem Tuncer, Sapienza University of Rome, Rome, Italy, sinem.tuncer@uniroma1.it