ArticleBlood advances2022
Differential regulation of CTLA4 expression through BTK-dependent and independent mechanisms in CLL.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Opportunities and challenges for cancer immunotherapy based on antigen cross-presentation.Annals of medicine · 2026Review
- Article
- A question of TiME: how microenvironmental interactions shape response to immunotherapy in CLL and Richter Transformation.Frontiers in immunology · 2025Review
- Article
- Overexpression of Potential Markers of Regulatory and Exhausted CD8International journal of molecular sciences · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Cytotoxic T lymphocyte antigen 4 (CTLA4) is a major immune checkpoint and target for cancer immunotherapy. Although originally discovered and primarily studied on T cells, its role on other cell types has also been recognized in recent years. Here we describe an unexpected interaction between ibrutinib (a targeted inhibitor of Bruton tyrosine kinase [BTK]) and CTLA4 expression on malignant chronic lymphocytic leukemia (CLL) cells. Although BTK itself does play a role in CTLA4 expression in CLL, we demonstrate that ibrutinib's main suppressive effect on CTLA4 protein expression and trafficking occurs through non-BTK targets influenced by this drug. This suppression is not seen in T cells, indicating a different mechanism of CTLA4 regulation in CLL vs T cells. Appreciating this distinct mechanism and the beneficial non-BTK effects of ibrutinib may contribute to understanding the immune benefits of ibrutinib treatment and lead to therapeutic approaches to improve immune function in patients with CLL by suppressing CTLA4 expression.
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