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An antibody against human interleukin-2 showing minimal binding to neonatal Fc receptor: Potent anti-tumor activity and reduced systemic toxicity in mice.
Eur J Pharmacol
January 2025
School of Life Science and Biopharmaceuticals, Shenyang Pharmaceutical University, 103 Culture Road, Shenhe District, Shenyang, Liaoning, 110016, China; Shenyang Sunshine Pharmaceuticals Co., Ltd, Economic and Technological Development Zone, Shenyang, Liaoning, 110027, China.
The anti-tumor efficacy of immune checkpoint inhibitors can be enhanced by combining them with interleukin-2 (IL-2), which promotes the clonal expansion of antigen-activated CD8 T cells and natural killer cells. However, IL-2 can simultaneously bind to endothelial cells and regulatory T cells to induce adverse and immunosuppressive effects. Such off-target binding can be inhibited by co-administering IL-2 with anti-IL-2 antibodies, but these antibodies can interact with neonatal Fc receptor to protect the IL-2 from lysosomal degradation, leading to substantial toxicity.
View Article and Find Full Text PDFWiskott-Aldrich syndrome protein maintains regulatory T cell tolerance by modulating their surface IL-2 receptor levels.
J Autoimmun
December 2024
National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Child Rare Diseases in Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China; Division of Rheumatology and Immunology, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. Electronic address:
Wiskott-Aldrich syndrome (WAS) is an X-linked immunodeficiency condition caused by ablation of functional WAS protein (WASP) expression, and associated with susceptibility to infections, eczema, and autoimmunity. Regulatory T cell (Treg) defects are an important cause of autoimmunity in WAS. Currently, the mechanisms underlying cytoskeleton involvement in Treg-regulated autoimmunity remain unclear, and WAS is an excellent model for investigation of this question.
View Article and Find Full Text PDFArticle Synopsis
- ANV419 Development
- : ANV419 is a novel fusion protein that combines IL-2 with an antibody to specifically activate certain immune cells while minimizing side effects commonly seen with traditional IL-2, like aldesleukin.
- Selective Immune Response
- : The fusion protein preferentially boosts the population of CD8 T cells and natural killer (NK) cells, demonstrating strong anti-tumor effects and improved tolerance levels in clinical testing, especially in mouse models.
- Clinical Potential
- : With a favorable half-life and manageable dosing, ANV419 is being tested in Phase 1/2 clinical trials for treating various cancers, potentially offering patients a safer and more effective alternative to existing IL-
Phase 1 first-in-human dose-escalation study of ANV419 in patients with relapsed/refractory advanced solid tumors.
J Immunother Cancer
November 2023
Early Drug Development Unit, Vall d'Hebron Institute of Oncology, Barcelona, Spain.
Background: ANV419 is a stable antibody-cytokine fusion protein consisting of interleukin-2 (IL-2) fused to an anti-IL-2 monoclonal antibody that sterically hinders binding of IL-2 to the α subunit of its receptor but has selective affinity for the receptor βγ subunits. Thus, ANV419 preferentially stimulates CD8 effector T cells and natural killer cells which are associated with tumor killing, while minimizing the activation of immunosuppressive regulatory T cells.
Methods: ANV419-001 is an open-label, multicenter, phase 1 study to evaluate the safety, tolerability, maximum tolerated dose (MTD) and recommended phase 2 dose (RP2D) of ANV419.
Effector-Phase IL-2 Signals Drive Th1 Effector and Memory Responses Dependently and Independently of TCF-1.
J Immunol
February 2024
Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84112.
Following viral infection, CD4+ T cell differentiation is tightly regulated by cytokines and TCR signals. Although most activated CD4+ T cells express IL-2Rα after lymphocytic choriomeningtis virus infection, by day 3 postinfection, only half of activated T cells maintain expression. IL-2Rα at this time point distinguishes precursors for terminally differentiated Th1 cells (IL-2Rαhi) from precursors for Tfh cells and memory T cells (IL-2Rαlo) and is linked to strong TCR signals.
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