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Article ; Online: Microglia in Central Nervous System Inflammation and Multiple Sclerosis Pathology.

Voet, Sofie / Prinz, Marco / van Loo, Geert

2018 Volume 25, Issue 2, Page(s) 112–123

Abstract: Microglia are the resident macrophages of the central nervous system (CNS). They have important physiological functions in maintaining tissue homeostasis but also contribute to CNS pathology. Microglia respond to changes in the microenvironment, and the ... ...

Abstract	Microglia are the resident macrophages of the central nervous system (CNS). They have important physiological functions in maintaining tissue homeostasis but also contribute to CNS pathology. Microglia respond to changes in the microenvironment, and the resulting reactive phenotype can be very diverse, with both neuroinflammatory and neuroprotective properties, illustrating the plasticity of these cells. Recent progress in understanding the autoimmune neuroinflammatory disease multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis suggests major roles for microglia in the disease, which have drastically changed our view on the function of microglia in MS.
MeSH term(s)	Animals ; Central Nervous System/immunology ; Central Nervous System/pathology ; Humans ; Inflammation/immunology ; Inflammation/pathology ; Microglia/immunology ; Microglia/pathology ; Multiple Sclerosis/immunology ; Multiple Sclerosis/pathology
Language	English
Publishing date	2018-12-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036490-8
ISSN	1471-499X ; 1471-4914
ISSN (online)	1471-499X
ISSN	1471-4914
DOI	10.1016/j.molmed.2018.11.005
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Article ; Online: Inflammasomes in neuroinflammatory and neurodegenerative diseases.

Voet, Sofie / Srinivasan, Sahana / Lamkanfi, Mohamed / van Loo, Geert

EMBO molecular medicine

2019 Volume 11, Issue 6

Abstract: Neuroinflammation and neurodegeneration often result from the aberrant deposition of aggregated host proteins, including amyloid-β, α-synuclein, and prions, that can activate inflammasomes. Inflammasomes function as intracellular sensors of both ... ...

Abstract	Neuroinflammation and neurodegeneration often result from the aberrant deposition of aggregated host proteins, including amyloid-β, α-synuclein, and prions, that can activate inflammasomes. Inflammasomes function as intracellular sensors of both microbial pathogens and foreign as well as host-derived danger signals. Upon activation, they induce an innate immune response by secreting the inflammatory cytokines interleukin (IL)-1β and IL-18, and additionally by inducing pyroptosis, a lytic cell death mode that releases additional inflammatory mediators. Microglia are the prominent innate immune cells in the brain for inflammasome activation. However, additional CNS-resident cell types including astrocytes and neurons, as well as infiltrating myeloid cells from the periphery, express and activate inflammasomes. In this review, we will discuss current understanding of the role of inflammasomes in common degenerative diseases of the brain and highlight inflammasome-targeted strategies that may potentially treat these diseases.
MeSH term(s)	Animals ; Brain/immunology ; Brain/pathology ; Humans ; Immunity, Innate ; Inflammasomes/immunology ; Interleukin-18/immunology ; Interleukin-1beta/immunology ; Microglia/immunology ; Microglia/pathology ; Neurodegenerative Diseases/immunology ; Neurodegenerative Diseases/pathology ; alpha-Synuclein/immunology
Chemical Substances	IL18 protein, human ; IL1B protein, human ; Inflammasomes ; Interleukin-18 ; Interleukin-1beta ; SNCA protein, human ; alpha-Synuclein
Language	English
Publishing date	2019-04-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.201810248
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Article ; Online: Inflammasome signaling is dispensable for ß-amyloid-induced neuropathology in preclinical models of Alzheimer's disease.

Frontiers in immunology

2024 Volume 15, Page(s) 1323409

Abstract: Background: Alzheimer's disease (AD) is the most common neurodegenerative disorder affecting memory and cognition. The disease is accompanied by an abnormal deposition of ß-amyloid plaques in the brain that contributes to neurodegeneration and is known ... ...

Abstract	Background: Alzheimer's disease (AD) is the most common neurodegenerative disorder affecting memory and cognition. The disease is accompanied by an abnormal deposition of ß-amyloid plaques in the brain that contributes to neurodegeneration and is known to induce glial inflammation. Studies in the Methods: Here, we evaluated the Results: Microglia-specific deletion of the inflammasome regulator A20 and inflammasome effector protease caspase-1 in the Conclusion: Collectively, these results question a generalizable role for inflammasome activation in preclinical amyloid-only models of neuroinflammation.
MeSH term(s)	Mice ; Animals ; Alzheimer Disease/pathology ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor/genetics ; Neuroinflammatory Diseases ; Mice, Transgenic ; Amyloid ; Amyloidogenic Proteins
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Amyloid ; Amyloidogenic Proteins
Language	English
Publishing date	2024-01-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1323409
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Article ; Online: S100B Is a Potential Disease Activity Marker in Nonsegmental Vitiligo.

Speeckaert, Reinhart / Voet, Sofie / Hoste, Esther / van Geel, Nanja

The Journal of investigative dermatology

2017 Volume 137, Issue 7, Page(s) 1445–1453

Abstract: Vitiligo is a chronic skin condition characterized by progressive depigmentation of the skin. S100B is a damage-associated molecular pattern protein expressed in melanocytes that has been proposed as a marker of melanocyte cytotoxicity. Although the use ... ...

Abstract	Vitiligo is a chronic skin condition characterized by progressive depigmentation of the skin. S100B is a damage-associated molecular pattern protein expressed in melanocytes that has been proposed as a marker of melanocyte cytotoxicity. Although the use of S100B as a biomarker in melanoma is well established, to our knowledge its association with vitiligo activity has not yet been investigated. Here, we show that S100B serum levels were significantly increased in patients with active nonsegmental vitiligo and strongly correlated with the affected body surface area. Prospective follow-up showed a predictive value of serum S100B levels on disease progression. In vitro experiments using repeated freeze-thaw procedures showed an intracellular up-regulation of S100B in normal and vitiligo melanocytes before an extensive release in the environment. This phenomenon may explain the increased S100B serum values in the active phase of vitiligo. In a monobenzone-induced vitiligo mouse model we could show the potential of S100B inhibition as a therapeutic strategy in vitiligo. In conclusion, this report shows the possible use of S100B as a biomarker for disease activity in vitiligo. Our data suggest that this damage-associated molecular pattern protein could play a substantial role in the pathogenesis of vitiligo and may be a potential new target for treatment.
MeSH term(s)	Adult ; Animals ; Biomarkers/metabolism ; Disease Models, Animal ; Disease Progression ; Enzyme-Linked Immunosorbent Assay ; Female ; Flow Cytometry ; Gene Expression Regulation ; Humans ; Immunohistochemistry ; Male ; Melanocytes/metabolism ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Prospective Studies ; RNA/genetics ; S100 Calcium Binding Protein beta Subunit/biosynthesis ; S100 Calcium Binding Protein beta Subunit/genetics ; Vitiligo/metabolism ; Young Adult
Chemical Substances	Biomarkers ; S100 Calcium Binding Protein beta Subunit ; S100B protein, human ; RNA (63231-63-0)
Language	English
Publishing date	2017-02-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2017.01.033
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Article ; Online: OTULIN Prevents Liver Inflammation and Hepatocellular Carcinoma by Inhibiting FADD- and RIPK1 Kinase-Mediated Hepatocyte Apoptosis.

Verboom, Lien / Martens, Arne / Priem, Dario / Hoste, Esther / Sze, Mozes / Vikkula, Hanna / Van Hove, Lisette / Voet, Sofie / Roels, Jana / Maelfait, Jonathan / Bongiovanni, Laura / de Bruin, Alain / Scott, Charlotte L / Saeys, Yvan / Pasparakis, Manolis / Bertrand, Mathieu J M / van Loo, Geert

Cell reports

2020 Volume 30, Issue 7, Page(s) 2237–2247.e6

Abstract: Inflammatory signaling pathways are tightly regulated to avoid chronic inflammation and the development of disease. OTULIN is a deubiquitinating enzyme that controls inflammation by cleaving linear ubiquitin chains generated by the linear ubiquitin chain ...

Abstract	Inflammatory signaling pathways are tightly regulated to avoid chronic inflammation and the development of disease. OTULIN is a deubiquitinating enzyme that controls inflammation by cleaving linear ubiquitin chains generated by the linear ubiquitin chain assembly complex. Here, we show that ablation of OTULIN in liver parenchymal cells in mice causes severe liver disease which is characterized by liver inflammation, hepatocyte apoptosis, and compensatory hepatocyte proliferation, leading to steatohepatitis, fibrosis, and hepatocellular carcinoma (HCC). Genetic ablation of Fas-associated death domain (FADD) completely rescues and knockin expression of kinase inactive receptor-interacting protein kinase 1 (RIPK1) significantly protects mice from developing liver disease, demonstrating that apoptosis of OTULIN-deficient hepatocytes triggers disease pathogenesis in this model. Finally, we demonstrate that type I interferons contribute to disease in hepatocyte-specific OTULIN-deficient mice. Our study reveals the critical importance of OTULIN in protecting hepatocytes from death, thereby preventing the development of chronic liver inflammation and HCC.
MeSH term(s)	Animals ; Apoptosis/physiology ; CHO Cells ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Cricetulus ; Endopeptidases/metabolism ; Fas-Associated Death Domain Protein/antagonists & inhibitors ; Fas-Associated Death Domain Protein/metabolism ; Hepatitis/genetics ; Hepatitis/metabolism ; Hepatitis/pathology ; Humans ; Interferon Type I/metabolism ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptor-Interacting Protein Serine-Threonine Kinases/antagonists & inhibitors ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Signal Transduction
Chemical Substances	Fadd protein, mouse ; Fas-Associated Death Domain Protein ; Interferon Type I ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk1 protein, mouse (EC 2.7.11.1) ; Endopeptidases (EC 3.4.-) ; gumby protein, mouse (EC 3.4.-)
Language	English
Publishing date	2020-02-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2020.01.028
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Article ; Online: Two distinct ubiquitin-binding motifs in A20 mediate its anti-inflammatory and cell-protective activities.

Nature immunology

2020 Volume 21, Issue 4, Page(s) 381–387

Abstract: Protein ubiquitination regulates protein stability and modulates the composition of signaling complexes. A20 is a negative regulator of inflammatory signaling, but the molecular mechanisms involved are ill understood. Here, we generated Tnfaip3 gene- ... ...

Abstract	Protein ubiquitination regulates protein stability and modulates the composition of signaling complexes. A20 is a negative regulator of inflammatory signaling, but the molecular mechanisms involved are ill understood. Here, we generated Tnfaip3 gene-targeted A20 mutant mice bearing inactivating mutations in the zinc finger 7 (ZnF7) and ZnF4 ubiquitin-binding domains, revealing that binding to polyubiquitin is essential for A20 to suppress inflammatory disease. We demonstrate that a functional ZnF7 domain was required for recruiting A20 to the tumor necrosis factor receptor 1 (TNFR1) signaling complex and to suppress inflammatory signaling and cell death. The combined inactivation of ZnF4 and ZnF7 phenocopied the postnatal lethality and severe multiorgan inflammation of A20-deficient mice. Conditional tissue-specific expression of mutant A20 further revealed the key role of ubiquitin-binding in myeloid and intestinal epithelial cells. Collectively, these results demonstrate that the anti-inflammatory and cytoprotective functions of A20 are largely dependent on its ubiquitin-binding properties.
MeSH term(s)	Animals ; Epithelial Cells/metabolism ; Humans ; Inflammation/metabolism ; Mice ; Mice, Inbred C57BL ; Myeloid Cells/metabolism ; Polyubiquitin/metabolism ; Protein Binding/physiology ; Signal Transduction/physiology ; Tumor Necrosis Factor alpha-Induced Protein 3/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Ubiquitin/metabolism ; Ubiquitination/physiology ; Zinc Fingers/physiology
Chemical Substances	Tumor Necrosis Factor-alpha ; Ubiquitin ; Polyubiquitin (120904-94-1) ; Tumor Necrosis Factor alpha-Induced Protein 3 (EC 3.4.19.12) ; Tnfaip3 protein, mouse (EC 3.4.22.-)
Language	English
Publishing date	2020-03-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-020-0621-9
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Pharmacological inhibition of MALT1 protease activity protects mice in a mouse model of multiple sclerosis.

Mc Guire, Conor / Elton, Lynn / Wieghofer, Peter / Staal, Jens / Voet, Sofie / Demeyer, Annelies / Nagel, Daniel / Krappmann, Daniel / Prinz, Marco / Beyaert, Rudi / van Loo, Geert

Journal of neuroinflammation

2014 Volume 11, Page(s) 124

Abstract: Background: The paracaspase mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) is crucial for lymphocyte activation through signaling to the transcription factor NF-κB. Besides functioning as a scaffold signaling protein, MALT1 ... ...

Abstract	Background: The paracaspase mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) is crucial for lymphocyte activation through signaling to the transcription factor NF-κB. Besides functioning as a scaffold signaling protein, MALT1 also acts as a cysteine protease that specifically cleaves a number of substrates and contributes to specific T cell receptor-induced gene expression. Recently, small molecule inhibitors of MALT1 proteolytic activity were identified and shown to have promising anticancer properties in subtypes of B cell lymphoma. However, information on the therapeutic potential of small compound inhibitors that target MALT1 protease activity in autoimmunity is still lacking. Methods: The present study aimed to elucidate whether MALT1 protease inhibitors are also useful in the treatment of lymphocyte-mediated autoimmune pathologies such as multiple sclerosis (MS). For this, we studied the therapeutic potential of a recently identified inhibitor of MALT1 protease activity, the phenothiazine derivative mepazine, in the context of experimental autoimmune encephalomyelitis (EAE), the main animal model for MS. Results: We demonstrate that administration of mepazine prophylactically or after disease onset, can attenuate EAE. Importantly, while complete absence of MALT1 affects the differentiation of regulatory T (Treg) cells in vivo, the MALT1 protease inhibitor mepazine did not affect Treg development. Conclusions: Altogether, these data indicate that small molecule inhibitors of MALT1 not only hold great promise for the treatment of B cell lymphomas but also for autoimmune disorders such as MS.
MeSH term(s)	Animals ; Antigens, CD/metabolism ; Caspases/metabolism ; Cell Differentiation/drug effects ; Cells, Cultured ; Cytokines/genetics ; Cytokines/metabolism ; Disease Models, Animal ; Encephalitis/chemically induced ; Encephalitis/drug therapy ; Encephalomyelitis, Autoimmune, Experimental/chemically induced ; Encephalomyelitis, Autoimmune, Experimental/drug therapy ; Follow-Up Studies ; Lymphocyte Activation ; Mice ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein ; Multiple Sclerosis/chemically induced ; Multiple Sclerosis/drug therapy ; Myelin-Oligodendrocyte Glycoprotein/toxicity ; NF-kappa B/metabolism ; Neoplasm Proteins/metabolism ; Peptide Fragments/toxicity ; Phenothiazines/therapeutic use ; Spinal Cord/drug effects ; Spinal Cord/metabolism ; Spinal Cord/pathology ; T-Lymphocytes/drug effects
Chemical Substances	Antigens, CD ; Cytokines ; Myelin-Oligodendrocyte Glycoprotein ; NF-kappa B ; Neoplasm Proteins ; Peptide Fragments ; Phenothiazines ; myelin oligodendrocyte glycoprotein (35-55) ; mepazine (60-89-9) ; Caspases (EC 3.4.22.-) ; Malt1 protein, mouse (EC 3.4.22.-) ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein (EC 3.4.22.-)
Language	English
Publishing date	2014-07-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/1742-2094-11-124
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Article ; Online: Cardiovascular and pharmacological implications of haem-deficient NO-unresponsive soluble guanylate cyclase knock-in mice.

Thoonen, Robrecht / Cauwels, Anje / Decaluwe, Kelly / Geschka, Sandra / Tainsh, Robert E / Delanghe, Joris / Hochepied, Tino / De Cauwer, Lode / Rogge, Elke / Voet, Sofie / Sips, Patrick / Karas, Richard H / Bloch, Kenneth D / Vuylsteke, Marnik / Stasch, Johannes-Peter / Van de Voorde, Johan / Buys, Emmanuel S / Brouckaert, Peter

Nature communications

2015 Volume 6, Page(s) 8482

Abstract: Oxidative stress, a central mediator of cardiovascular disease, results in loss of the prosthetic haem group of soluble guanylate cyclase (sGC), preventing its activation by nitric oxide (NO). Here we introduce Apo-sGC mice expressing haem-free sGC. Apo- ... ...

Abstract	Oxidative stress, a central mediator of cardiovascular disease, results in loss of the prosthetic haem group of soluble guanylate cyclase (sGC), preventing its activation by nitric oxide (NO). Here we introduce Apo-sGC mice expressing haem-free sGC. Apo-sGC mice are viable and develop hypertension. The haemodynamic effects of NO are abolished, but those of the sGC activator cinaciguat are enhanced in apo-sGC mice, suggesting that the effects of NO on smooth muscle relaxation, blood pressure regulation and inhibition of platelet aggregation require sGC activation by NO. Tumour necrosis factor (TNF)-induced hypotension and mortality are preserved in apo-sGC mice, indicating that pathways other than sGC signalling mediate the cardiovascular collapse in shock. Apo-sGC mice allow for differentiation between sGC-dependent and -independent NO effects and between haem-dependent and -independent sGC effects. Apo-sGC mice represent a unique experimental platform to study the in vivo consequences of sGC oxidation and the therapeutic potential of sGC activators.
MeSH term(s)	Animals ; Benzoates/pharmacology ; Blood Pressure/drug effects ; Cardiovascular System/drug effects ; Cardiovascular System/metabolism ; Gene Knock-In Techniques ; Guanylate Cyclase/genetics ; Heme/genetics ; Hypertension/genetics ; Hypotension/chemically induced ; Hypotension/genetics ; Mice ; Mice, Transgenic ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/metabolism ; Nitric Oxide/metabolism ; Oxidative Stress/drug effects ; Platelet Aggregation/drug effects ; Receptors, Cytoplasmic and Nuclear/genetics ; Soluble Guanylyl Cyclase ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	Benzoates ; Receptors, Cytoplasmic and Nuclear ; Tumor Necrosis Factor-alpha ; Nitric Oxide (31C4KY9ESH) ; BAY 58-2667 (329773-35-5) ; Heme (42VZT0U6YR) ; Guanylate Cyclase (EC 4.6.1.2) ; Soluble Guanylyl Cyclase (EC 4.6.1.2)
Language	English
Publishing date	2015-10-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/ncomms9482
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Article ; Online: A20 critically controls microglia activation and inhibits inflammasome-dependent neuroinflammation.

Voet, Sofie / Mc Guire, Conor / Hagemeyer, Nora / Martens, Arne / Schroeder, Anna / Wieghofer, Peter / Daems, Carmen / Staszewski, Ori / Vande Walle, Lieselotte / Jordao, Marta Joana Costa / Sze, Mozes / Vikkula, Hanna-Kaisa / Demeestere, Delphine / Van Imschoot, Griet / Scott, Charlotte L / Hoste, Esther / Gonçalves, Amanda / Guilliams, Martin / Lippens, Saskia /

Libert, Claude / Vandenbroucke, Roos E / Kim, Ki-Wook / Jung, Steffen / Callaerts-Vegh, Zsuzsanna / Callaerts, Patrick / de Wit, Joris / Lamkanfi, Mohamed / Prinz, Marco / van Loo, Geert

Nature communications

2018 Volume 9, Issue 1, Page(s) 2036

Abstract: Microglia, the mononuclear phagocytes of the central nervous system (CNS), are important for the maintenance of CNS homeostasis, but also critically contribute to CNS pathology. Here we demonstrate that the nuclear factor kappa B (NF-κB) regulatory ... ...

Abstract	Microglia, the mononuclear phagocytes of the central nervous system (CNS), are important for the maintenance of CNS homeostasis, but also critically contribute to CNS pathology. Here we demonstrate that the nuclear factor kappa B (NF-κB) regulatory protein A20 is crucial in regulating microglia activation during CNS homeostasis and pathology. In mice, deletion of A20 in microglia increases microglial cell number and affects microglial regulation of neuronal synaptic function. Administration of a sublethal dose of lipopolysaccharide induces massive microglia activation, neuroinflammation, and lethality in mice with microglia-confined A20 deficiency. Microglia A20 deficiency also exacerbates multiple sclerosis (MS)-like disease, due to hyperactivation of the Nlrp3 inflammasome leading to enhanced interleukin-1β secretion and CNS inflammation. Finally, we confirm a Nlrp3 inflammasome signature and IL-1β expression in brain and cerebrospinal fluid from MS patients. Collectively, these data reveal a critical role for A20 in the control of microglia activation and neuroinflammation.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Animals ; Brain/immunology ; Brain/pathology ; Disease Models, Animal ; Female ; Humans ; Inflammasomes/immunology ; Interleukin-1beta/metabolism ; Lipopolysaccharides/immunology ; Male ; Mice ; Microglia/immunology ; Microglia/pathology ; Middle Aged ; Multiple Sclerosis/cerebrospinal fluid ; Multiple Sclerosis/immunology ; Multiple Sclerosis/pathology ; NLR Family, Pyrin Domain-Containing 3 Protein/immunology ; Signal Transduction/immunology ; Tumor Necrosis Factor alpha-Induced Protein 3/genetics ; Tumor Necrosis Factor alpha-Induced Protein 3/immunology ; Tumor Necrosis Factor alpha-Induced Protein 3/metabolism
Chemical Substances	IL1B protein, human ; IL1B protein, mouse ; Inflammasomes ; Interleukin-1beta ; Lipopolysaccharides ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 protein, human ; Nlrp3 protein, mouse ; TNFAIP3 protein, human (EC 3.4.19.12) ; Tumor Necrosis Factor alpha-Induced Protein 3 (EC 3.4.19.12) ; Tnfaip3 protein, mouse (EC 3.4.22.-)
Language	English
Publishing date	2018-05-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-018-04376-5
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