Rapid Review·General Pathology

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NEOPLASIA

T2High yield

Immune Checkpoints & Checkpoint Inhibitors

P218

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Key takeaways

a signal that dials down T-cell activation, and therefore the immune response against tumor cells. Tumors upregulate them to evade killing.
PD-1 on T cells binds PD-L1 or PD-L2 on tumor cells or on immune cells in the tumor microenvironment → T-cell dysfunction, known as exhaustion.
  • Anti-PD-1: cemiplimab, nivolumab, pembrolizumab.
  • Anti-PD-L1: atezolizumab, durvalumab, avelumab.
CTLA-4 on T cells outcompetes CD28 for B7 on APCs → the costimulatory second signal is lost → the T cell is never activated.
  • Anti-CTLA-4: ipilimumab.
releasing the brake causes immune-related adverse events, namely colitis, hepatitis, dermatitis, pneumonitis, and autoimmune endocrinopathies such as hypophysitis and thyroiditis.

How it's tested

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High-yield images1
Immune checkpoint interactions: PD-1 (T cell)/PD-L1 (tumor) and CTLA-4/B7 inhibit T-cell activation; checkpoint inhibitors (anti-PD-1 nivolumab/pembrolizumab/cemiplimab, anti-PD-L1 atezolizumab/durvalumab/avelumab, anti-CTLA-4 ipilimumab) restore antitumor T-cell responses.

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What receptors on tumor cells interacts with PD-1 on T cells to cause T-cell dysfunction?

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