IL-2-mediated hepatotoxicity: knowledge gap identification based on the irAOP concept-Reference-Cited by-同舟云学术

IL-2-mediated hepatotoxicity: knowledge gap identification based on the irAOP concept

Published:2024-01-26 Issue:sup1 Volume:21 Page:
ISSN:1547-691X
Container-title:Journal of Immunotoxicology
language:en
Short-container-title:Journal of Immunotoxicology

Author:

Roser Luise A.¹,Sakellariou Christina²,Lindstedt Malin²^ORCID,Neuhaus Vanessa³⁴,Dehmel Susann³⁴,Sommer Charline³⁴,Raasch Martin⁵,Flandre Thierry⁶,Roesener Sigrid⁷,Hewitt Philip⁷,Parnham Michael J.¹⁸,Sewald Katherina³⁴,Schiffmann Susanne⁸^ORCID

Affiliation:

1. Fraunhofer Institute for Translational Medicine and Pharmacology (ITMP), Frankfurt am Main, Germany

2. Department of Immunotechnology, Lund University, Lund, Sweden

3. Fraunhofer Institute for Toxicology and Experimental Medicine (ITEM), Preclinical Pharmacology and In-Vitro Toxicology, Hannover, Germany

4. Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Member of the Fraunhofer Cluster of Excellence Immune-Mediated Diseases CIMD, Hannover, Germany

5. Dynamic42 GmbH, Jena, Germany

6. Translational Medicine, Novartis Institutes of Biomedical Research, Basel, Switzerland

7. Chemical and Preclinical Safety, Merck Healthcare KGaA, Darmstadt, Germany

8. EpiEndo Pharmaceuticals ehf, Reykjavík, Iceland

Funder

Innovative Medicines Initiative 2 Joint Undertaking

Publisher

Informa UK Limited

Link

https://www.tandfonline.com/doi/pdf/10.1080/1547691X.2024.2332177

Reference210 articles.

1. Revisiting IL-2: Biology and therapeutic prospects

2. Clinical immunology Expression of CD11b and CD18 on polymorphonuclear neutrophils stimulated with interleukin-2

3. Induction of natural killer cell migration by monocyte chemotactic protein−1, −2 and −3

4. The role of cytokines, adhesion molecules, and chemokines in interleukin-2-induced lymphocytic infiltration in C57BL/6 mice.

5. Perforin, Fas/Fas ligand, and TNF-alpha pathways as specific and bystander killing mechanisms of hepatitis C virus-specific human CTL.

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