Researchers from Fudan University, the Second Military Medical University and other institutions confirmed in the new study that CBP / p300 linking NF-Κb and CREB regulates CD59 expression, protecting cells from complement attacks. The research findings were published online on December 12 in the Journal of Biochemistry (JBC).
Professor Weiguo Hu from Fudan University and Associate Professor Xuhui Zhou of the Second Military Medical University are co-corresponding authors of this paper. Professor Hu Weiguo's main research direction is the basic and clinical related research of the complement system, as well as tumor-related applied translational research. Associate Professor Zhou Xuhui has long been engaged in clinical work and related research in spinal surgery, especially scoliosis.
The complement system is an important part of innate immunity and a bridge connecting innate immunity and acquired immunity. Its basic physiological functions include the removal of cellular debris, apoptotic / dead cells and immune complexes, and invading pathogens, and further coordination of the entire immune and inflammatory response, while the function further evolves and participates in synaptic maturation, angiogenesis, hematopoietic stem cells The migration, tissue regeneration and lipid metabolism are widely involved in the occurrence and development of different immunoreactive diseases, inflammation, tumors, neurodegenerative diseases, etc.
The C3b / iC3b cleavage product after the activation of the complement system can "mark" the cells to be cleared, and the corresponding receptors expressed on the surface of the innate immune cell membrane can be combined to remove these abnormal cellular components; Factor, also has a strong chemokine function, can induce a strong immune response in the local activation of complement; the membrane attack complex (Membrane Attack Complex, MAC) formed in the final stage of complement activation can directly cleave the pathogen to be cleared , Can also induce extensive and complex downstream signaling pathways.
In order to prevent the damaging effect on normal cells after complement activation, membrane-bound complement regulatory proteins (mCRP) such as CD46, CD55 and CD59 are expressed on the surface of the host cell membrane, which inhibits complement activation at different stages of complement activation and protects host cells. By constitutively and inducibly expressing CD59, host cells can limit MAC assembly to protect themselves from harmful damage caused by complement. However, the potential regulatory mechanism of CD59 is not yet clear.
In this new article, the researchers confirmed that the widely expressed transcription factor Sp1 may regulate the constitutive expression of CD59, and during the activation of complement triggered by lipopolysaccharide (LPS), CBP / p300 connects NF-κB and enhancer The binding protein CREB induces up-regulation of CD59, thus enabling the host to defend against MAC-mediated further destruction. The researchers confirmed that treatment with LPS, TNF-α, and complement activators SC5b-9 and C5a one by one can increase CD59 expression by activating NF-κB and CREB signaling pathways.
These findings have identified a novel CD59 regulatory mechanism related to CBP / p300, NF-κB and CREB, thus providing some potential therapeutic targets for controlling various complement-related human diseases.
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