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IRAK3-mediated suppression of pro-inflammatory MyD88/IRAK signaling affects disease severity in acute pancreatitis

Scientific reports, 2023-07, Vol.13 (1), p.10833-10833, Article 10833

2023

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In mouse chronic pancreatitis CD25+FOXP3+ regulatory T cells control pancreatic fibrosis by suppression of the type 2 immune response

Nature communications, 2022-08, Vol.13 (1), p.4502-4502, Article 4502

2022

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Immune response mechanisms in acute and chronic pancreatitis: strategies for therapeutic intervention

Frontiers in immunology, 2023-10, Vol.14, p.1279539-1279539

2023

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Systemic Bile Acids Affect the Severity of Acute Pancreatitis in Mice Depending on Their Hydrophobicity and the Disease Pathogenesis

International journal of molecular sciences, 2022-11, Vol.23 (21), p.13592

2022

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Mobilization of CD11b+/Ly6chi monocytes causes multi organ dysfunction syndrome in acute pancreatitis

Frontiers in immunology, 2022-10, Vol.13, p.991295-991295

2022

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Pro-inflammatory cytokines of the IL-6 family induce regulatory T-cells and determine the severity of acute pancreatitis

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2023-11, Vol.23, p.e5-e5

2023

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NLRP3 Inflammasome Regulates Development of Systemic Inflammatory Response and Compensatory Anti-Inflammatory Response Syndromes in Mice With Acute Pancreatitis

Gastroenterology (New York, N.Y. 1943), 2020-01, Vol.158 (1), p.253-269.e14

2020

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The tissue remodeling of chronic pancreatitis is driven by a local type 2 immune response

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2022-11, Vol.22, p.e26-e26

2022

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Tu1203: BILE ACIDS MODULATE THE SEVERITY OF ACUTE PANCREATITIS DEPENDING ON THEIR HYDROPHOBICITY AND BY INTERACTING WITH CCK1 RECEPTOR

Gastroenterology (New York, N.Y. 1943), 2022-05, Vol.162 (7), p.S-912

2022

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Role of Bile Acids and Bile Salts in Acute Pancreatitis: From the Experimental to Clinical Studies

Pancreas, 2021-01, Vol.50 (1), p.3

2021

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Experimental pancreatitis is characterized by rapid T cell activation, Th2 differentiation that parallels disease severity, and improvement after CD4+ T cell depletion

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2020-12, Vol.20 (8), p.1637-1647

2020

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Pancreatitis severity in mice with impaired CFTR function but pancreatic sufficiency is mediated via ductal and inflammatory cells‐Not acinar cells

Journal of cellular and molecular medicine, 2021-05, Vol.25 (10), p.4658-4670

2021

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Interleukin 33 regulates Th2 T-cell differentiation and macrophage polarization during acute pancreatitis

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2019-06, Vol.19, p.S101-S101

2019

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The depletion of Foxp3+/CD25+ regulatory T cells drives a Th2 immune response and reduces severity in a mouse model of acute pancreatitis

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2019-06, Vol.19, p.S26-S26

2019

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Depletion of CD4+ T-helper cells reduces pancreatic damage in two models of acute pancreatitis

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2018-06, Vol.18 (4), p.S30-S30

2018

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Non classical macrophage polarization regulates the immune response during acute pancreatitis

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2018-06, Vol.18 (4), p.S126-S127

2018

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Macrophage-derived cytokines of the IL1 family simultaneously regulate pro- and anti-inflammation during severe acute pancreatitis

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2019-06, Vol.19, p.S5-S5

2019

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Adaptive immune response during acute pancreatitis is regulated by NLRP3 inflammasome activation via interleukin 18

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2018-06, Vol.18 (4), p.S87-S88

2018

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Versorgungssituation von CIDP-Patienten in neun deutschen Zentren des Neuritis Netzes

Nervenarzt, 2023-04, Vol.94 (4), p.320-326

2023

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Public health situation of CIDP patients in nine German centers-neuritis network Germany

Nervenarzt, 2023-04, Vol.94 (4), p.320-326

2023

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Phosphorylation of serine 774 of the neural cell adhesion molecule is necessary for cyclic adenosine monophosphate response element binding protein activation and neurite outgrowth

Journal of neuroscience research, 2012-08, Vol.90 (8), p.1577-1582

2012

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Phosphorylation of Serine 774 of the Neural Cell Adhesion Molecule (NCAM) Is Involved in the Interaction with Collapsin Response Mediator Protein-2

Neurochemical research, 2013-06, Vol.38 (6), p.1229-1235

2013

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Role of collapsin response mediator protein-2 in neurite outgrowth of PC12 cells

Neuroreport, 2010-06, Vol.21 (9), p.641-645

2010

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IRAK3-mediated suppression of pro-inflammatory MyD88/IRAK signaling affects disease severity in acute pancreatitis

In mouse chronic pancreatitis CD25+FOXP3+ regulatory T cells control pancreatic fibrosis by suppression of the type 2 immune response

Immune response mechanisms in acute and chronic pancreatitis: strategies for therapeutic intervention

Systemic Bile Acids Affect the Severity of Acute Pancreatitis in Mice Depending on Their Hydrophobicity and the Disease Pathogenesis

Mobilization of CD11b+/Ly6chi monocytes causes multi organ dysfunction syndrome in acute pancreatitis

Pro-inflammatory cytokines of the IL-6 family induce regulatory T-cells and determine the severity of acute pancreatitis

NLRP3 Inflammasome Regulates Development of Systemic Inflammatory Response and Compensatory Anti-Inflammatory Response Syndromes in Mice With Acute Pancreatitis

The tissue remodeling of chronic pancreatitis is driven by a local type 2 immune response

Activated regulatory T-cells promote duodenal bacterial translocation into necrotic areas in severe acute pancreatitis

Tu1203: BILE ACIDS MODULATE THE SEVERITY OF ACUTE PANCREATITIS DEPENDING ON THEIR HYDROPHOBICITY AND BY INTERACTING WITH CCK1 RECEPTOR

Role of Bile Acids and Bile Salts in Acute Pancreatitis: From the Experimental to Clinical Studies

Experimental pancreatitis is characterized by rapid T cell activation, Th2 differentiation that parallels disease severity, and improvement after CD4+ T cell depletion

Pancreatitis severity in mice with impaired CFTR function but pancreatic sufficiency is mediated via ductal and inflammatory cells‐Not acinar cells

Interleukin 33 regulates Th2 T-cell differentiation and macrophage polarization during acute pancreatitis

The depletion of Foxp3+/CD25+ regulatory T cells drives a Th2 immune response and reduces severity in a mouse model of acute pancreatitis

Depletion of CD4+ T-helper cells reduces pancreatic damage in two models of acute pancreatitis

Non classical macrophage polarization regulates the immune response during acute pancreatitis

Macrophage-derived cytokines of the IL1 family simultaneously regulate pro- and anti-inflammation during severe acute pancreatitis

Adaptive immune response during acute pancreatitis is regulated by NLRP3 inflammasome activation via interleukin 18

Versorgungssituation von CIDP-Patienten in neun deutschen Zentren des Neuritis Netzes

Public health situation of CIDP patients in nine German centers-neuritis network Germany

Phosphorylation of serine 774 of the neural cell adhesion molecule is necessary for cyclic adenosine monophosphate response element binding protein activation and neurite outgrowth

Phosphorylation of Serine 774 of the Neural Cell Adhesion Molecule (NCAM) Is Involved in the Interaction with Collapsin Response Mediator Protein-2

Role of collapsin response mediator protein-2 in neurite outgrowth of PC12 cells

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