Activation-induced cell death

Definition

Activation-induced cell death (AICD) is a mechanism through which activated lymphocytes undergo apoptosis after prolonged stimulation, particularly following their encounter with antigens. This process is crucial for maintaining immune homeostasis, preventing overactivation of the immune system, and eliminating self-reactive T cells that could lead to autoimmunity. AICD plays a key role in both central and peripheral tolerance by ensuring that only properly regulated immune responses persist.

5 Must Know Facts For Your Next Test

1. AICD is primarily mediated by the interaction of the T cell receptor (TCR) with its specific antigen, leading to signals that trigger apoptosis.
2. The key molecules involved in AICD include Fas (CD95) and its ligand (FasL), which are critical for initiating the apoptotic pathway in activated T cells.
3. AICD helps eliminate excess activated T cells after an immune response, reducing the risk of tissue damage and preventing chronic inflammation.
4. This process also contributes to the clonal deletion of self-reactive T cells during thymic selection, enhancing central tolerance mechanisms.
5. Failure in AICD can lead to autoimmune diseases, as it may allow self-reactive lymphocytes to persist and cause tissue damage.

Review Questions

• How does activation-induced cell death contribute to the regulation of T cell populations during an immune response?
  • Activation-induced cell death plays a vital role in regulating T cell populations by inducing apoptosis in activated T cells after they have completed their function. This mechanism prevents excessive accumulation of T cells, which could lead to autoimmune reactions or chronic inflammation. By ensuring that only necessary T cells remain after an immune response, AICD helps maintain balance and homeostasis within the immune system.
• Discuss the importance of Fas and FasL in the mechanism of activation-induced cell death.
  • Fas and FasL are crucial components in the process of activation-induced cell death. When activated T cells express Fas, they can engage with FasL, which triggers a signaling cascade leading to apoptosis. This interaction serves as a primary mechanism for eliminating excess activated T cells, thereby preventing overactivation of the immune system. The proper functioning of Fas and FasL is essential for maintaining immune tolerance and preventing autoimmune diseases.
• Evaluate how dysfunctions in activation-induced cell death mechanisms can lead to autoimmune diseases and discuss potential therapeutic strategies.
  • Dysfunction in activation-induced cell death mechanisms can result in the survival of self-reactive T cells that should otherwise undergo apoptosis. This can lead to an overactive immune response against the body's own tissues, manifesting as autoimmune diseases. Potential therapeutic strategies include enhancing AICD pathways using agents that promote Fas signaling or developing treatments aimed at specifically targeting and eliminating autoreactive T cells. Understanding these mechanisms can help design more effective therapies for managing autoimmune conditions.

Related terms

Apoptosis: A form of programmed cell death that occurs in multicellular organisms, characterized by specific cellular changes and the elimination of cells without causing inflammation.

T cell activation: The process by which T cells are stimulated to proliferate and differentiate in response to an antigen, typically involving interactions with antigen-presenting cells.

Peripheral tolerance: The mechanisms that prevent harmful immune responses against self-antigens outside of the thymus, helping to maintain immune homeostasis and prevent autoimmunity.