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TNFSF15 disease-risk polymorphism increases pattern-recognition receptor-induced signaling through caspase-8–induced IL-1

Proceedings of the National Academy of Sciences - PNAS, 2014-09, Vol.111 (37), p.13451-13456

2014

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Human LACC1 increases innate receptor-induced responses and a LACC1 disease-risk variant modulates these outcomes

Nature communications, 2017-06, Vol.8 (1), p.15614-13, Article 15614

2017

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IRF5 and IRF5 Disease-Risk Variants Increase Glycolysis and Human M1 Macrophage Polarization by Regulating Proximal Signaling and Akt2 Activation

Cell reports (Cambridge), 2016-08, Vol.16 (9), p.2442-2455

2016

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Twist1 and Twist2 Induce Human Macrophage Memory upon Chronic Innate Receptor Treatment by HDAC-Mediated Deacetylation of Cytokine Promoters

The Journal of immunology (1950), 2019-06, Vol.202 (11), p.3297-3308

2019

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LACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes

Cell reports (Cambridge), 2019-12, Vol.29 (13), p.4525-4539.e4

2019

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IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine

Nature (London), 2012-11, Vol.491 (7423), p.259-263

2012

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Secretory Mediators Regulate Nod2-Induced Tolerance in Human Macrophages

Gastroenterology (New York, N.Y. 1943), 2011-01, Vol.140 (1), p.231-241

2011

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MTMR3 risk allele enhances innate receptor-induced signaling and cytokines by decreasing autophagy and increasing caspase-1 activation

Proceedings of the National Academy of Sciences - PNAS, 2015-08, Vol.112 (33), p.10461-10466

2015

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TAM receptor-dependent regulation of SOCS3 and MAPKs contributes to proinflammatory cytokine downregulation following chronic NOD2 stimulation of human macrophages

The Journal of immunology (1950), 2015-02, Vol.194 (4), p.1928-1937

2015

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Chronic stimulation of Nod2 mediates tolerance to bacterial products

Proceedings of the National Academy of Sciences - PNAS, 2007-12, Vol.104 (49), p.19440-19445

2007

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Pattern Recognition Receptor Signaling in Human Dendritic Cells is Enhanced by ICOS Ligand and Modulated by the Crohn’s Disease ICOSLG Risk Allele

Immunity (Cambridge, Mass.), 2014-05, Vol.40 (5), p.734-746

2014

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ErbB4 signaling stimulates pro-inflammatory macrophage apoptosis and limits colonic inflammation

Cell death & disease, 2017-02, Vol.8 (2), p.e2622-e2622

2017

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INAVA-ARNO complexes bridge mucosal barrier function with inflammatory signaling

eLife, 2018-10, Vol.7

2018

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E3 Ubiquitin ligase ZNRF4 negatively regulates NOD2 signalling and induces tolerance to MDP

Nature communications, 2017-06, Vol.8 (1), p.15865-16, Article 15865

2017

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A TPL2 (MAP3K8) disease-risk polymorphism increases TPL2 expression thereby leading to increased pattern recognition receptor-initiated caspase-1 and caspase-8 activation, signalling and cytokine secretion

Gut, 2016-11, Vol.65 (11), p.1799-1811

2016

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IL23 induces IL23R recycling and amplifies innate receptor-induced signalling and cytokines in human macrophages, and the IBD-protective IL23R R381Q variant modulates these outcomes

Gut, 2020-02, Vol.69 (2), p.264

2020

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IRF5 risk polymorphisms contribute to interindividual variance in pattern recognition receptor-mediated cytokine secretion in human monocyte-derived cells

The Journal of immunology (1950), 2012-06, Vol.188 (11), p.5348-5356

2012

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Distinct Roles for Nod2 Protein and Autocrine Interleukin-1β in Muramyl Dipeptide-induced Mitogen-activated Protein Kinase Activation and Cytokine Secretion in Human Macrophages

The Journal of biological chemistry, 2011-07, Vol.286 (30), p.26440-26449

2011

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The E3 ubiquitin ligase RNF186 and RNF186 risk variants regulate innate receptor-induced outcomes

Proceedings of the National Academy of Sciences - PNAS, 2021-08, Vol.118 (32), p.1

2021

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Nod2-Induced Autocrine Interleukin-1 Alters Signaling by ERK and p38 to Differentially Regulate Secretion of Inflammatory Cytokines

Gastroenterology (New York, N.Y. 1943), 2012-12, Vol.143 (6), p.1530-1543

2012

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Erratum: E3 Ubiquitin ligase ZNRF4 negatively regulates NOD2 signalling and induces tolerance to MDP

Nature communications, 2017-08, Vol.8 (1), p.16141-16141, Article 16141

2017

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Disease Risk-Associated Genetic Variants in STAT1 and STAT4 Function in a Complementary Manner to Increase Pattern-Recognition Receptor-Induced Outcomes in Human Macrophages

The Journal of immunology (1950), 2020-09, Vol.205 (5), p.1406-1418

2020

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Ubiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response

The Journal of clinical investigation, 2021-09, Vol.131 (17)

2021

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Myeloid Cell-Intrinsic IRF5 Promotes T Cell Responses through Multiple Distinct Checkpoints In Vivo, and IRF5 Immune-Mediated Disease Risk Variants Modulate These Myeloid Cell Functions

The Journal of immunology (1950), 2020-08, Vol.205 (4), p.1024-1038

2020

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An inflammatory bowel disease-risk variant in INAVA decreases pattern recognition receptor-induced outcomes

The Journal of clinical investigation, 2017-06, Vol.127 (6), p.2192-2205

2017

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TNFSF15 disease-risk polymorphism increases pattern-recognition receptor-induced signaling through caspase-8–induced IL-1

Human LACC1 increases innate receptor-induced responses and a LACC1 disease-risk variant modulates these outcomes

IRF5 and IRF5 Disease-Risk Variants Increase Glycolysis and Human M1 Macrophage Polarization by Regulating Proximal Signaling and Akt2 Activation

Twist1 and Twist2 Induce Human Macrophage Memory upon Chronic Innate Receptor Treatment by HDAC-Mediated Deacetylation of Cytokine Promoters

LACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes

IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine

Secretory Mediators Regulate Nod2-Induced Tolerance in Human Macrophages

MTMR3 risk allele enhances innate receptor-induced signaling and cytokines by decreasing autophagy and increasing caspase-1 activation

TAM receptor-dependent regulation of SOCS3 and MAPKs contributes to proinflammatory cytokine downregulation following chronic NOD2 stimulation of human macrophages

Chronic stimulation of Nod2 mediates tolerance to bacterial products

Pattern Recognition Receptor Signaling in Human Dendritic Cells is Enhanced by ICOS Ligand and Modulated by the Crohn’s Disease ICOSLG Risk Allele

ErbB4 signaling stimulates pro-inflammatory macrophage apoptosis and limits colonic inflammation

INAVA-ARNO complexes bridge mucosal barrier function with inflammatory signaling

E3 Ubiquitin ligase ZNRF4 negatively regulates NOD2 signalling and induces tolerance to MDP

A TPL2 (MAP3K8) disease-risk polymorphism increases TPL2 expression thereby leading to increased pattern recognition receptor-initiated caspase-1 and caspase-8 activation, signalling and cytokine secretion

IL23 induces IL23R recycling and amplifies innate receptor-induced signalling and cytokines in human macrophages, and the IBD-protective IL23R R381Q variant modulates these outcomes

IRF5 risk polymorphisms contribute to interindividual variance in pattern recognition receptor-mediated cytokine secretion in human monocyte-derived cells

Distinct Roles for Nod2 Protein and Autocrine Interleukin-1β in Muramyl Dipeptide-induced Mitogen-activated Protein Kinase Activation and Cytokine Secretion in Human Macrophages

The E3 ubiquitin ligase RNF186 and RNF186 risk variants regulate innate receptor-induced outcomes

Nod2-Induced Autocrine Interleukin-1 Alters Signaling by ERK and p38 to Differentially Regulate Secretion of Inflammatory Cytokines

Erratum: E3 Ubiquitin ligase ZNRF4 negatively regulates NOD2 signalling and induces tolerance to MDP

Disease Risk-Associated Genetic Variants in STAT1 and STAT4 Function in a Complementary Manner to Increase Pattern-Recognition Receptor-Induced Outcomes in Human Macrophages

Ubiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response

Myeloid Cell-Intrinsic IRF5 Promotes T Cell Responses through Multiple Distinct Checkpoints In Vivo, and IRF5 Immune-Mediated Disease Risk Variants Modulate These Myeloid Cell Functions

An inflammatory bowel disease-risk variant in INAVA decreases pattern recognition receptor-induced outcomes

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