How Do You Spell DECAY ACCELERATING FACTOR?

Pronunciation: [dɪkˈe͡ɪ ɐksˈɛləɹˌe͡ɪtɪŋ fˈaktə] (IPA)

Decay Accelerating Factor (DAF) is a protein found on the surface of human cells, particularly those in the complement system, which helps protect against pathogens. The correct spelling of DAF uses the IPA phonetic transcription system to indicate the pronunciation. The word "decay" is pronounced /dɪˈkeɪ/, while "accelerating" is pronounced /əkˈsɛləretɪŋ/. Finally, "factor" is pronounced /ˈfæktər/. Together, the phonetic spelling of DAF is /dɪˈkeɪ əkˈsɛləretɪŋ ˈfæktər/.

DECAY ACCELERATING FACTOR Meaning and Definition

1. Decay Accelerating Factor (DAF) is a term used in the field of immunology to refer to a membrane-bound protein that plays a crucial role in the regulation of the immune system. It is also known as CD55, which stands for cluster of differentiation 55, a protein found on the surface of various cells in the body.

   The primary function of DAF is to protect cells from being attacked and destroyed by the immune system. It acts as a complement regulatory protein, meaning that it prevents the overactivation of the complement system – a part of the immune response that aids in the destruction of foreign invaders.

   This protein accomplishes its regulatory role by inhibiting the spontaneous activation of complement proteins on the surface of self-cells. Specifically, DAF interferes with the formation and amplification of the C3 and C5 convertases, which are crucial enzymes involved in the complement cascade. By doing so, it helps maintain the balance between a controlled immune response against pathogens and the prevention of unnecessary damage to healthy cells.

   Failure or deficiency of decay accelerating factor can lead to enhanced complement activation and subsequent tissue damage. This has been associated with various autoimmune diseases, such as hemolytic anemia and paroxysmal nocturnal hemoglobinuria.

   In conclusion, Decay Accelerating Factor is a membrane-bound protein that regulates the activation of the complement system, protecting self-cells from immune-mediated destruction and maintaining immune homeostasis.

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