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5. ZC3H12C expression in DCs is necessary to prevent lymphadenopathy of skin-draining lymph nodes

Author

Clayer, E., Frank, D., Anderton, H., Zhang, S., Kueh, A., Heim, V., Nutt, S.L., Chopin, M., and Bouillet, P.

Subjects
Rna-binding Protein, Regnase 3, Tumour Necrosis Factor, Dendritic Cells, Lymphadenopathy
Abstract

The role of RNA-binding proteins of the CCCH-containing family in regulating pro-inflammatory cytokine production and inflammation is increasingly recognized. We have identified ZC3H12C (Regnase-3) as a potential post-transcriptional regulator of Tumor necrosis factor expression and have investigated its role in vivo by generating Zc3h12c-deficient mice that express GFP instead of ZC3H12C. Zc3h12c-deficient mice develop hypertrophic lymph nodes. In the immune system, ZC3H12C expression is mostly restricted to the dendritic cell (DC) populations, and we show that DC-restricted ZC3H12C depletion is sufficient to cause lymphadenopathy. ZC3H12C can regulate Tnf mRNA stability via its RNAse activity in vitro, and we confirmed the role of Tnf in the development of lymphadenopathy. Finally, we found that loss of ZC3H12C did not impact the outcome of skin inflammation in the imiquimod-induced murine model of psoriasis, despite Zc3h12c being identified as a risk factor for psoriasis susceptibility in several GWAS studies. Our data suggest a role for ZC3H12C in DC-driven skin homeostasis.

Published
2022

9. The Manor of Bardsea

Author

Anderton, H I

Abstract

Transactions of the Cumberland & Westmorland Antiquarian & Archaeological Society, 12, 216-261

Published
2017
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11. TRAF2 regulates TNF and NF-κB signalling to suppress apoptosis and skin inflammation independently of Sphingosine kinase-1

Author

Etemadi, N, Chopin, M, Anderton, H, Tanzer, M C, Rickard, J A, Abeysekera, W, Hall, C, Spall, S K, Wang, B, Xiong, Y, HLa, T, Pitson, S M, Bonder, C S, Wong, W W-L, Ernst, M, Smyth, G K, Vaux, D L, Nutt, S L, Nachbur, U, Silke, J, University of Zurich, and Silke, J

Subjects
1300 General Biochemistry, Genetics and Molecular Biology, 2400 General Immunology and Microbiology, 570 Life sciences, biology, 2800 General Neuroscience, 610 Medicine & health, 10263 Institute of Experimental Immunology
Published
2015

12. Inhibitor of apoptosis (IAP) proteins limit RIP3 dependent IL-1 activation

Author

Vince, J E, Wong, W Wei-Lynn, Gentle, I E, Lawlor, K E, Allam, R, O'Reilly, L, Mason, K, Gross, O, Ma, S, Guarda, G, Anderton, H, Castillo, R, Häcker, G, Silke, J, Tschopp, J, and University of Zurich

Subjects
2403 Immunology, 2723 Immunology and Allergy, 570 Life sciences, biology, 610 Medicine & health, 2725 Infectious Diseases, 10263 Institute of Experimental Immunology
Published
2012

13. IAPs must limit activation of RIP kinases by TNF Receptor 1 to prevent embryonic lethality

Author

Moulin, M, Anderton, H, Voss, A K, Thomas, T, Wong, W W L, Bankovacki, A, Feltham, R, Chau, D, Cook, W D, Silke, J, Vaux, D L, University of Zurich, and Vaux, D L

Subjects
General Immunology and Microbiology, 1300 General Biochemistry, Genetics and Molecular Biology, 2400 General Immunology and Microbiology, General Neuroscience, General Biochemistry, 1312 Molecular Biology, 570 Life sciences, biology, 2800 General Neuroscience, 610 Medicine & health, Genetics and Molecular Biology, 10263 Institute of Experimental Immunology, Molecular Biology
Published
2012

14. In TNF-stimulated cells, RIPK1 promotes cell survival by stabilizing TRAF2 and cIAP1, which limits induction of non-canonical NF-kappaB and activation of caspase-8

Author

Gentle, I E, Wong, W W L, Evans, J M, Bankovacki, A, Cook, W D, Khan, N R, Nachbur, U, Rickard, J, Anderton, H, Moulin, M, Lluis, J M, Moujalled, D M, Silke, J, Vaux, D L, and University of Zurich

Subjects
1307 Cell Biology, 1303 Biochemistry, 1312 Molecular Biology, 570 Life sciences, biology, 610 Medicine & health, 10263 Institute of Experimental Immunology
Published
2011

15. Linear ubiquitination prevents inflammation and regulates immune signalling

Author

Gerlach, B, Cordier, S M, Schmukle, A C, Emmerich, C H, Rieser, E, Haas, T L, Webb, A I, Rickard, J A, Anderton, H, Wong, W W L, Nachbur, U, Gangoda, L, Warnken, U, Purcell, A W, Silke, J, Walczak, H, University of Zurich, and Walczak, H

Subjects
1000 Multidisciplinary, 570 Life sciences, biology, 610 Medicine & health, 10263 Institute of Experimental Immunology
Published
2011

22. RIPK1 is not essential for TNFR1-induced activation of NF-κB.

Author

Wong, W. W.-L., Gentle, I. E., Nachbur, U., Anderton, H., Vaux, D. L., and Silke, J.

Subjects
CELL death, APOPTOSIS, CONNECTIVE tissue cells, PHOSPHOTRANSFERASES, PROTEIN kinases
Abstract

On TNF binding, receptor-interacting protein kinase 1 (RIPK1) is recruited to the cytoplasmic domain of TNFR1, at which it becomes ubiquitylated and serves as a platform for recruitment and activation of NEMO/IKK1/IKK2 and TAK1/TAB2. RIPK1 is commonly thought to be required for the activation of canonical NF-κB and for inhibition TNFR1-induced apoptosis. RIPK1 has, however, also been reported to be essential for TNFR1-induced apoptosis when cIAPs are depleted. To determine the role of RIPK1 in TNF/IAP antagonist-induced death, we compared wild type (WT) and RIPK1−/− mouse embryonic fibroblasts (MEFs) treated with these compounds. On being treated with TNF plus IAP antagonist, RIPK1−/− MEFs survived, unlike WT MEFs, demonstrating a killing activity of RIPK1. Surprisingly, however, on being treated with TNF alone, RIPK1−/− MEFs activated canonical NF-κB and did not die. Furthermore, several cell types from E18 RIPK1−/− embryos seem to activate NF-κB in response to TNF. These data indicate that models proposing that RIPK1 is essential for TNFR1 to activate canonical NF-κB are incorrect. [ABSTRACT FROM AUTHOR]

Published
2010
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