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Polyamines and hypusination are important for Clostridioides difficile toxin B (TcdB)-mediated activation of group 3 innate lymphocytes (ILC3s)

Infection and immunity, 2023-11, Vol.91 (11), p.e0023623-e0023623

2023

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Modulation of innate lymphoid cells by enteric bacterial pathogens

Frontiers in immunology, 2023-07, Vol.14, p.1219072-1219072

2023

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Cx3cr1 controls kidney resident macrophage heterogeneity

Frontiers in immunology, 2023-05, Vol.14, p.1082078

2023

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The Polyamine Putrescine Is a Positive Regulator of Group 3 Innate Lymphocyte Activation

ImmunoHorizons, 2023-01, Vol.7 (1), p.41-48

2023

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Group 3 innate lymphocytes (ILC3s) upregulate IL-22 in response to elevated intracellular cAMP levels

Cytokine (Philadelphia, Pa.), 2022-05, Vol.153, p.155862-155862, Article 155862

2022

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Clostridioides difficile Toxin B Activates Group 3 Innate Lymphocytes

Infection and immunity, 2022-04, Vol.90 (4), p.e0007322

2022

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IL-22 Binding Protein (IL-22BP) in the Regulation of IL-22 Biology

Frontiers in immunology, 2021-11, Vol.12, p.766586-766586

Zenewicz, Lauren A

2021

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E3 Ubiquitin Ligase Von Hippel-Lindau Protein Promotes Th17 Differentiation

The Journal of immunology (1950), 2020-08, Vol.205 (4), p.1009-1023

2020

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Glucocorticoids Inhibit Group 3 Innate Lymphocyte IL-22 Production

The Journal of immunology (1950), 2018-08, Vol.201 (4), p.1267-1274

2018

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Glucocorticoids inhibit group 3 innate lymphocyte IL-22 production1

The Journal of immunology (1950), 2018-07, Vol.201 (4), p.1267-1274

2018

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IL-22: There Is a Gap in Our Knowledge

ImmunoHorizons, 2018-07, Vol.2 (6), p.198-207

Zenewicz, Lauren A

2018

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IL-22 deficiency increases CD4 T cell responses to mucosal immunization

Vaccine, 2018-06, Vol.36 (25), p.3694-3700

2018

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Glucocorticoids inhibit group 3 innate lymphocyte IL-22 production

The Journal of immunology (1950), 2018-05, Vol.200 (1_Supplement), p.43-43.1

2018

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Bacillus anthracis lethal toxin negatively modulates ILC3 function through perturbation of IL-23-mediated MAPK signaling

PLoS pathogens, 2017-10, Vol.13 (10), p.e1006690-e1006690

2017

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Hypoxic modulation of hepatocyte responses to the cytokine interleukin‐22

Immunology and cell biology, 2017-04, Vol.95 (4), p.380-387

2017

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Oxygen Levels and Immunological Studies

Frontiers in immunology, 2017-03, Vol.8, p.324-324

Zenewicz, Lauren A

2017

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Transcription Factor HIF-1α Controls Expression of the Cytokine IL-22 in CD4 T Cells

The Journal of immunology (1950), 2016-10, Vol.197 (7), p.2646-2652

2016

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Defective Intestinal Mucin-Type O-Glycosylation Causes Spontaneous Colitis-Associated Cancer in Mice

Gastroenterology (New York, N.Y. 1943), 2016-07, Vol.151 (1), p.152-164.e11

2016

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The transcription factor HIF1α controls expression of the cytokine IL-22 in CD4 T cells

The Journal of immunology (1950), 2016-05, Vol.196 (1_Supplement), p.120-120.3

2016

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Correction: Corrigendum: NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells

Nature (London), 2016-02, Vol.530 (7591), p.504-504

2016

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Corrigendum: NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells

Nature (London), 2016-02, Vol.530 (7591), p.504-504

2016

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IL-22 deficiency alters colonic microbiota to be transmissible and colitogenic

The Journal of immunology (1950), 2013-05, Vol.190 (10), p.5306-5312

2013

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Excessive Th1 responses due to the absence of TGF-β signaling cause autoimmune diabetes and dysregulated Treg cell homeostasis

Proceedings of the National Academy of Sciences - PNAS, 2013-04, Vol.110 (17), p.6961-6966

2013

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Excessive Th1 responses due to the absence of TGF-[Beta] signaling cause autoimmune diabetes and dysregulated Treg cell homeostasis

Proceedings of the National Academy of Sciences - PNAS, 2013-04, Vol.110 (17), p.6961

2013

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Interleukin-22 deficiency alters colonic microbiota to be transmissible and colitogenic

The Journal of immunology (1950), 2013-04, Vol.190 (10), p.5306-5312

2013

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Polyamines and hypusination are important for Clostridioides difficile toxin B (TcdB)-mediated activation of group 3 innate lymphocytes (ILC3s)

Modulation of innate lymphoid cells by enteric bacterial pathogens

Cx3cr1 controls kidney resident macrophage heterogeneity

The Polyamine Putrescine Is a Positive Regulator of Group 3 Innate Lymphocyte Activation

Group 3 innate lymphocytes (ILC3s) upregulate IL-22 in response to elevated intracellular cAMP levels

Clostridioides difficile Toxin B Activates Group 3 Innate Lymphocytes

IL-22 Binding Protein (IL-22BP) in the Regulation of IL-22 Biology

E3 Ubiquitin Ligase Von Hippel-Lindau Protein Promotes Th17 Differentiation

Glucocorticoids Inhibit Group 3 Innate Lymphocyte IL-22 Production

Glucocorticoids inhibit group 3 innate lymphocyte IL-22 production1

IL-22: There Is a Gap in Our Knowledge

IL-22 deficiency increases CD4 T cell responses to mucosal immunization

Glucocorticoids inhibit group 3 innate lymphocyte IL-22 production

Bacillus anthracis lethal toxin negatively modulates ILC3 function through perturbation of IL-23-mediated MAPK signaling

Hypoxic modulation of hepatocyte responses to the cytokine interleukin‐22

Oxygen Levels and Immunological Studies

Transcription Factor HIF-1α Controls Expression of the Cytokine IL-22 in CD4 T Cells

Defective Intestinal Mucin-Type O-Glycosylation Causes Spontaneous Colitis-Associated Cancer in Mice

The transcription factor HIF1α controls expression of the cytokine IL-22 in CD4 T cells

Correction: Corrigendum: NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells

Corrigendum: NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells

IL-22 deficiency alters colonic microbiota to be transmissible and colitogenic

Excessive Th1 responses due to the absence of TGF-β signaling cause autoimmune diabetes and dysregulated Treg cell homeostasis

Excessive Th1 responses due to the absence of TGF-[Beta] signaling cause autoimmune diabetes and dysregulated Treg cell homeostasis

Interleukin-22 deficiency alters colonic microbiota to be transmissible and colitogenic

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