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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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Immune checkpoint receptors in autoimmunity.

Kelly P Burke1, Dillon G Patterson2, Dan Liang2

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Current Opinion in Immunology
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PubMed
Summary

Immune checkpoint receptors regulate T cell function and tolerance. Dysregulation or blockade of these receptors can lead to autoimmune diseases and immune-related adverse events.

Keywords:
AutoimmunityCheckpoint receptor ligandCheckpoint receptorsImmune related adverse event (irAE)PD-1PD-L1T cell tolerance

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Area of Science:

  • Immunology
  • Autoimmunity
  • Cancer Immunotherapy

Background:

  • Immune checkpoint receptors, including programmed cell death protein 1 (PD-1), cytotoxic T-lymphocyte associated protein 4 (CTLA-4), lymphocyte-activation gene 3 (LAG-3), and T cell immunoglobulin and ITIM domain (TIGIT), play critical roles in regulating T cell responses.
  • These receptors mediate immune tolerance, and their dysregulation can result in autoimmune syndromes.
  • Therapeutic blockade of immune checkpoints for cancer immunotherapy can paradoxically induce organ inflammation, known as immune-related adverse events (irAE), which mimic autoimmune conditions.

Purpose of the Study:

  • To review recent advances in understanding how immune checkpoint receptors regulate autoimmunity.
  • To highlight the connections between gene expression, T cell heterogeneity, and autoimmune regulation.
  • To explore the parallels between irAE and natural autoimmunity.

Main Methods:

  • Review of current literature on immune checkpoint receptors and autoimmunity.
  • Analysis of gene expression programs associated with checkpoint regulation.
  • Examination of T cell population heterogeneity in autoimmune contexts.
  • Comparison of mechanisms underlying irAE and spontaneous autoimmune diseases.

Main Results:

  • Immune checkpoint receptors exhibit distinct yet overlapping inhibitory functions on T cells.
  • Dysregulation of these receptors is linked to the breakdown of self-tolerance and autoimmune diseases.
  • Immune-related adverse events share significant parallels with natural autoimmunity, suggesting common underlying mechanisms.
  • Bidirectional functional interactions between immune checkpoint receptors and their ligands are crucial in these processes.

Conclusions:

  • Immune checkpoint receptors are key regulators of self-tolerance and autoimmunity.
  • Understanding the complex interplay between checkpoint receptors, T cell populations, and their ligands is essential for managing both autoimmune diseases and irAE.
  • Further research into these pathways may offer novel therapeutic strategies for both autoimmunity and cancer immunotherapy.