The emerging role of CTLA4 as a cell-extrinsic regulator of T cell responses

By L. Walker, D. Sansom. Nature reviews. Immunology, 2011

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Distinct cellular mechanisms underlie anti-CTLA-4 and anti-PD-1 checkpoint blockade (2017, positive): “Whereas CTLA-4 primarily attenuates T cell activation in the priming phase through cell intrinsic and extrinsic mechanisms, PD-1 primarily attenuates T cell activity in peripheral tissues through cell intrinsic mechanisms (Pardoll, 2012;Walker and Sansom, 2011).”
Autosomal-dominant immune dysregulation syndrome in humans with CTLA4 mutations (2014, positive): “Depletion of the co-stimulatory ligands CD80 and CD86 by CTLA-4 reduces antigen presenting cell-mediated activation of conventional T cells via CD28, resulting in dominant suppression of T cell activation 20 .”
A clinical trial of CTLA-4 blockade with tremelimumab in patients with hepatocellular carcinoma and chronic hepatitis C. (2013, background): “CTLA-4 blockade releases this brake and enhances T cell activation and proliferation through various mechanisms still under intense study [11,12].”
Review of Indications of FDA-Approved Immune Checkpoint Inhibitors per NCCN Guidelines with the Level of Evidence (2020, background): “As it has a higher affinity for CD80 (B7-1) and CD86 (B7-2), it outcompetes CD28, which leads to a reduction in the release of pro-effector cytokines such as IL-12 and cytotoxic enzymes such as perforin and granzyme B [22,23].”