The complement decay-accelerating factor, also named CD55 or DAF, is a membrane protein encoded by the CD55 gene in humans. In general, DAF can be detected among hematopoietic and non-hematopoietic cells. Studies have shown that DAF presents important roles in the regulation of the complement system on the cell surface. It recognizes C4b produced during C4 (classical or lectin pathway) activation and C3b fragment produced during C3 (alternative pathway) activation. The interaction of DAF with C4b prevents the formation of the C4b2a C3 convertase, while the interaction with C3b prevents the formation of C3bBb C3 convertase. New research shows that the functional site of DAF, also known as complement control protein repeats (CCPs), is contained in four repeating units of approximately 61 amino acids.
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Published Data
Fig. 1 DAF reduces ischemia-induced neuronal cell death.1
The activated complement system is known to play a role in promoting neuroinflammation and neurodegeneration following exposure to hypoxic-ischemic injury. Therefore, inhibiting the complement activation cascade could be a promising therapeutic strategy for treating ischemic brain injury. Decay-accelerating factor (DAF), also referred to as CD55, can limit the local generation of C3a and C5a, as well as the production of the membrane attack complex. Research has focused on the capacity of DAF to safeguard primary cultured neuronal cells from sodium cyanide (NaCN)-induced hypoxia, a condition that triggers cell degeneration and apoptosis. Results indicated that DAF significantly reduced neuronal cell death and apoptosis under these hypoxic conditions. This is because complement activation is limited by DAF, which also inhibits the activity of the protein Src and caspase 9 and 3. Overall, this study supports the idea that inhibiting complement activation may serve as a neuroprotective strategy against ischemia/reperfusion injury in the central nervous.
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Reference
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Wang, Ying, et al. "Decay accelerating factor (CD55) protects neuronal cells from chemical hypoxia-induced injury." Journal of Neuroinflammation 7 (2010): 1-13. Distributed under Open Access license CC BY 2.0, without modification.
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