Cytotoxic T-lymphocyte antigen 4 (CTLA-4) is a protein receptor on T immune cells that prevents the cells from killing other cells, such as cancer cells. Blocking CTLA-4 with a specific antibody is an effective treatment for some cancers, but it can damage the heart. New research published in The FASEB Journal reveals the mechanisms involved in this side effect—a finding that could be used to help prevent it.
Cytotoxic T-lymphocyte antigen 4 (CTLA-4) is a protein receptor on T immune cells that prevents the cells from killing other cells, such as cancer cells. Blocking CTLA-4 with a specific antibody is an effective treatment for some cancers, but it can damage the heart. New research published in The FASEB Journal reveals the mechanisms involved in this side effect—a finding that could be used to help prevent it.
Experiments conducted in mice showed that blocking CTLA-4 activates certain T cells called Th17 cells, which increase inflammation. Inhibiting this activation reversed anti-CTLA-4–mediated heart damage.
“Targeting this axis could potentially offer a preventive or therapeutic strategy for managing cardiotoxicity in patients undergoing anti-CTLA-4-based immune checkpoint inhibitor therapy,” the authors wrote.
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About the Journal
The FASEB Journal publishes multidisciplinary research covering biology and biomedical sciences at every level of organization: atomic, molecular, cell, tissue, organ, organismic, and population. The journal’s scope includes the spectrum of biological and biomedical sciences as well as interdisciplinary research cutting across multiple fields and extending into related areas.
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Journal
The FASEB Journal
Article Title
Blocking CTLA-4 promotes pressure overload-induced heart failure via activating Th17 cells
Article Publication Date
7-Aug-2024
