Nrf2 Induces IL-17D to Mediate Tumor and Virus Surveillance

Saddawi‐Konefka, Robert; Seelige, Ruth; Gross, Emilie; Lévy, Eric; Searles, Stephen; Washington, Allen; Santosa, Endi K.; Liu, Beichen; O’Sullivan, Timothy E.; Harismendy, Olivier; Bui, Jack D.

doi:10.1016/j.celrep.2016.07.075

Cited by 115 publications

(130 citation statements)

References 55 publications

(79 reference statements)

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“…Similarly, the gene encoding the proinflammatory cytokine, IL-17D, contains AREs, and this NRF2-T helper (Th)17 axis seems to confer protection against tumorigenesis and viral infections (Saddawi-Konefka et al, 2016).…”

Section: A Key Role Of Nuclear Factor (Erythroid-derived 2)-like 2 Imentioning

confidence: 99%

Transcription Factor NRF2 as a Therapeutic Target for Chronic Diseases: A Systems Medicine Approach

et al. 2018

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Section: A Key Role Of Nuclear Factor (Erythroid-derived 2)-like 2 Imentioning

confidence: 99%

Transcription Factor NRF2 as a Therapeutic Target for Chronic Diseases: A Systems Medicine Approach

et al. 2018

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“…Interestingly, the stress-sensing protein NRF2 induces IL-17D expression in cancer cells. IL-17D-deficient mice displayed increased tumor growth when compared to wild type mice [147]. Recent studies have also linked IL-17D to the recruitment of NK cells into the tumor microenvironment and subsequent activation [148, 149].…”

Section: Il-17 Family Cytokines In Host Protection and Inflammationmentioning

confidence: 99%

Interleukin 17 Family Cytokines: Signaling Mechanisms, Biological Activities, and Therapeutic Implications

Monin

Gaffen

2017

Cold Spring Harb Perspect Biol

256

235

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The cytokines of the IL-17 family play a central role in the control of infections, especially extracellular fungi. Conversely, if unrestrained, these inflammatory cytokines contribute to the pathology in numerous autoimmune and chronic inflammatory conditions. Recent advances have led to the approval of IL-17A-blocking biologics for the treatment of moderate to severe plaque psoriasis, but much remains to be understood about the biological functions, regulation and signaling pathways downstream of these factors. In this review, we outline the current knowledge on signal transduction and known physiological activities of IL-17 family cytokines. We will highlight in particular the current understanding of these cytokines in the context of skin manifestations of disease.

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“…IL17D is a pro-inflammatory cytokine that binds to a yet unknown receptor and directs in vivo the intra-tissular recruitment of NK T-cells [64,65]. Of note, IL17D, as all the members of the IL17 family, is also a potent inducer of TGFB secretion in many cell types [66,67].…”

Section: Discussionmentioning

confidence: 99%

A Unique TGFB1-Driven Genomic Program Links Astrocytosis, Low-Grade Inflammation and Partial Demyelination in Periplaques of Spinal Cords from Progressive Multiple Sclerosis Patients

Nataf¹,

Barritault²,

Pays³

2017

Preprint

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Abstract:We previously reported that in multiple sclerosis (MS) patients with a progressive form of the disease, spinal cord periplaques extend distance away from plaque borders and are characterized by the co-occurrence of partial demyelination, astrocytosis and low-grade inflammation. However, transcriptomic analyses comparing periplaques to adjacent normal-appearing white matter (NAWM) areas did not allow providing a comprehensive view of molecular events in astrocytes vs oligodendrocytes. Here, we re-assessed our transcriptomic data with the aim of identifying functionally-relevant co-expression networks that would reflect astrocyte vs oligodendrocyte molecular signatures in periplaques. We identified an astrocytosis-related gene module comprising GFAP, the hub gene CX43/GJA1 and a set of transcripts forming a TGFB/SMAD1/SMAD2 genomic signature. Partial demyelination was characterized by a co-expression network which, besides myelin genes, comprised a highly significant number of translation/elongation-related genes. Interestingly, the main oligodendrocyte-related hub we identified was NDRG1, a gene previously shown to be specifically silenced in the NAWM of MS patients. This result indicated that NDRG1 down-regulation could be an important event in the process of periplaque partial demyelination. To establish a putative link between NDRG1 down-regulation and a cytokine/chemokine signature, we then sought to identify cytokine/chemokine genes whose mRNA levels inversely correlated with those of NDRG1. Following this approach we found 5 candidate immune-related genes whose up-regulation associated with NDRG1 down-regulation: TGFB1, PDGFC, . From these results we propose that in the spinal cord of MS patients with progressive forms of the disease, TGFB1 may Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted:

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Nrf2 Induces IL-17D to Mediate Tumor and Virus Surveillance

Cited by 115 publications

References 55 publications

Transcription Factor NRF2 as a Therapeutic Target for Chronic Diseases: A Systems Medicine Approach

Transcription Factor NRF2 as a Therapeutic Target for Chronic Diseases: A Systems Medicine Approach

Interleukin 17 Family Cytokines: Signaling Mechanisms, Biological Activities, and Therapeutic Implications

A Unique TGFB1-Driven Genomic Program Links Astrocytosis, Low-Grade Inflammation and Partial Demyelination in Periplaques of Spinal Cords from Progressive Multiple Sclerosis Patients

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