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Targeting T regulatory (Treg) cells in immunotherapy-resistant cancers.
Spiliopoulou, Pavlina; Kaur, Paramjit; Hammett, Tracey; Di Conza, Giusy; Lahn, Michael.
Afiliação
  • Spiliopoulou P; Department of Drug Development Program, Phase I Unit, Beatson West of Scotland Cancer Center, Glasgow G12 0YN, UK.
  • Kaur P; School of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK.
  • Hammett T; Department of Oncology Clinical Development, iOnctura SA, Geneva 1202, Switzerland.
  • Di Conza G; Department of Oncology Clinical Development, iOnctura SA, Geneva 1202, Switzerland.
  • Lahn M; Department of Oncology Clinical Development, iOnctura SA, Geneva 1202, Switzerland.
Cancer Drug Resist ; 7: 2, 2024.
Article em En | MEDLINE | ID: mdl-38318526
ABSTRACT
Primary or secondary (i.e., acquired) resistance is a common occurrence in cancer patients and is often associated with high numbers of T regulatory (Treg) cells (CD4+CD25+FOXP3+). The approval of ipilimumab and the development of similar pharmacological agents targeting cell surface proteins on Treg cells demonstrates that such intervention may overcome resistance in cancer patients. Hence, the clinical development and subsequent approval of Cytotoxic T Lymphocyte Antigen-4 (CTLA-4) targeting agents can serve as a prototype for similar agents. Such new agents aspire to be highly specific and have a reduced toxicity profile while increasing effector T cell function or effector T/T regulatory (Teff/Treg) ratio. While clinical development with large molecules has shown the greatest advancement, small molecule inhibitors that target immunomodulation are increasingly entering early clinical investigation. These new small molecule inhibitors often target specific intracellular signaling pathways [e.g., phosphoinositide-3-kinase delta (PI3K-δ)] that play an important role in regulating the function of Treg cells. This review will summarize the lessons currently applied to develop novel clinical agents that target Treg cells.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article