Decay-Accelerating Factor

Definition

Decay-accelerating factor (DAF) is a protein that plays a critical role in regulating the complement system by preventing the formation of the C3 convertase enzyme complex. By inhibiting this enzyme's activity, DAF helps to control complement activation, protecting host cells from damage that can occur due to excessive or uncontrolled complement activity. It is particularly important for maintaining self-tolerance and preventing damage to healthy tissues during immune responses.

5 Must Know Facts For Your Next Test

1. DAF is also known as CD55 and is expressed on the surface of various cell types, including endothelial cells and lymphocytes.
2. By inhibiting the C3 convertase, DAF prevents the opsonization and subsequent phagocytosis of host cells, thereby protecting them from complement-mediated damage.
3. Deficiencies or dysfunctions in DAF can lead to uncontrolled complement activation, which is associated with various autoimmune diseases and tissue damage.
4. DAF works in conjunction with other regulatory proteins, such as factor H and membrane cofactor protein (MCP), to maintain balance within the complement system.
5. The importance of DAF in maintaining self-tolerance highlights its role in preventing the development of conditions like hemolytic uremic syndrome and atypical hemolytic uremic syndrome.

Review Questions

• How does decay-accelerating factor function within the complement system, and why is this function important for protecting host cells?
  • Decay-accelerating factor (DAF) functions by inhibiting the formation of C3 convertase, which is essential for amplifying the complement response. This inhibition is crucial because it prevents the overactivation of the complement system, which can lead to damage of host tissues. By regulating complement activity, DAF ensures that immune responses target pathogens effectively while minimizing harm to healthy cells.
• Discuss how a deficiency in decay-accelerating factor might contribute to autoimmune diseases.
  • A deficiency in decay-accelerating factor (DAF) can lead to uncontrolled activation of the complement system, resulting in excessive inflammation and tissue damage. When DAF is not functioning properly, healthy cells may be mistakenly targeted by the immune system, contributing to the development of autoimmune diseases. This overactivation can cause conditions such as hemolytic uremic syndrome, where red blood cells are destroyed, leading to serious health complications.
• Evaluate the role of decay-accelerating factor in maintaining self-tolerance and its implications for immune regulation.
  • Decay-accelerating factor (DAF) plays a critical role in maintaining self-tolerance by preventing excessive complement activation on host cells. Its ability to inhibit C3 convertase ensures that immune responses are appropriately targeted and do not attack self-tissues. This regulation is vital in preventing autoimmune reactions, highlighting DAF's significance not only in immune defense against pathogens but also in preserving the integrity of healthy tissues. Dysfunctional DAF can disrupt this balance, leading to serious implications for immune regulation and increased susceptibility to autoimmune disorders.

Related terms

Complement System: A group of proteins that work together to enhance the immune response by marking pathogens for destruction and promoting inflammation.

C3 Convertase: An enzyme complex formed during the complement activation pathways that cleaves C3 into C3a and C3b, crucial for the amplification of the complement response.

Self-Tolerance: The ability of the immune system to recognize and not attack the body's own cells, preventing autoimmune reactions.