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Beyond the Role of CD55 As a Complement Component

Overview
Journal Immune Netw
Date 2018 Mar 6
PMID 29503741
Citations 48
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Abstract

The complement is a part of the immune system that plays several roles in removing pathogens. Despite the importance of the complement system, the exact role of each component has been overlooked because the complement system was thought to be a nonspecific humoral immune mechanism that worked against pathogens. Decay-accelerating factor (DAF or CD55) is a known inhibitor of the complement system and has recently attracted substantial attention due to its role in various diseases, such as cancer, protein-losing enteropathy, and malaria. Some protein-losing enteropathy cases are caused by CD55 deficiency, which leads to complement hyperactivation, malabsorption, and angiopathic thrombosis. In addition, CD55 has been reported to be an essential host receptor for infection by the malaria parasite. Moreover, CD55 is a ligand of the seven-span transmembrane receptor CD97. Since CD55 is present in various cells, the functional role of CD55 has been expanded by showing that CD55 is associated with a variety of diseases, including cancer, malaria, protein-losing enteropathy, paroxysmal nocturnal hemoglobinuria, and autoimmune diseases. This review summarizes the current understanding of CD55 and the role of CD55 in these diseases. It also provides insight into the development of novel drugs for the diagnosis and treatment of diseases associated with CD55.

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References
1.
Huser A, Rudolph M, Hofmann C . Incorporation of decay-accelerating factor into the baculovirus envelope generates complement-resistant gene transfer vectors. Nat Biotechnol. 2001; 19(5):451-5. DOI: 10.1038/88122. View

2.
Lin H, Stacey M, Saxby C, Knott V, Chaudhry Y, Evans D . Molecular analysis of the epidermal growth factor-like short consensus repeat domain-mediated protein-protein interactions: dissection of the CD97-CD55 complex. J Biol Chem. 2001; 276(26):24160-9. DOI: 10.1074/jbc.M101770200. View

3.
Nakagawa M, Mizuno M, Kawada M, Uesu T, Nasu J, Takeuchi K . Polymorphic expression of decay-accelerating factor in human colorectal cancer. J Gastroenterol Hepatol. 2001; 16(2):184-9. DOI: 10.1046/j.1440-1746.2001.02418.x. View

4.
Thurman J, Nester C . All Things Complement. Clin J Am Soc Nephrol. 2016; 11(10):1856-1866. PMC: 5053787. DOI: 10.2215/CJN.01710216. View

5.
Hamann J, Wishaupt J, van Lier R, Smeets T, Breedveld F, Tak P . Expression of the activation antigen CD97 and its ligand CD55 in rheumatoid synovial tissue. Arthritis Rheum. 1999; 42(4):650-8. DOI: 10.1002/1529-0131(199904)42:4<650::AID-ANR7>3.0.CO;2-S. View