scholarly journals Hijacking Complement Regulatory Proteins for Bacterial Immune Evasion

2016 ◽  
Vol 7 ◽  
Author(s):  
Elise S. Hovingh ◽  
Bryan van den Broek ◽  
Ilse Jongerius
2005 ◽  
Vol 187 (4) ◽  
pp. 1317-1323 ◽  
Author(s):  
John V. McDowell ◽  
Matthew E. Harlin ◽  
Elizabeth A. Rogers ◽  
Richard T. Marconi

ABSTRACT Factor H and factor H like-protein 1 (FHL-1) are complement regulatory proteins that serve as cofactors for the factor I-mediated cleavage of C3b. Some Lyme disease and relapsing fever spirochete species bind factor H to their surface to facilitate immune evasion. The Lyme disease spirochetes produce several factor H binding proteins (FHBPs) that form two distinct classes. Class I FHBPs (OspE orthologs and paralogs) bind only factor H, while class II FHBPs (BBA68) bind both factor H and FHL-1. BBA68 belongs to a large paralogous protein family, and of these paralogs, BBA69 is the member most closely related to BBA68. To determine if BBA69 can also bind factor H, recombinant protein was generated and tested for factor H binding. BBA69 did not exhibit factor H binding ability, suggesting that among family 54 paralogs, factor H binding is unique to BBA68. To identify the determinants of BBA68 that are involved in factor H binding, truncation and site-directed mutational analyses were performed. These analyses revealed that the factor H binding site is discontinuous and provide strong evidence that coiled-coil structural elements are involved in the formation of the binding site.


2013 ◽  
Vol 41 (1) ◽  
pp. 258-262 ◽  
Author(s):  
Jameel M. Inal ◽  
Ephraim A. Ansa-Addo ◽  
Sigrun Lange

The release of extracellular vesicles, whether MVs (microvesicles) or exosomes, from host cells or intracellular pathogens is likely to play a significant role in the infection process. Host MVs may fuse with pathogen surfaces to deliver host complement regulatory proteins. They may also deliver cytokines that enhance invasion. Decoy functions are also possible. Whereas host MVs may direct pathogens away from their target cells, pathogen MVs may in turn redirect complement membrane-attack complexes away from their target pathogen. An understanding of the mechanisms of this interplay, bringing about both immune evasion and enhanced invasion, will help to direct future research with a view to rendering pathogens more susceptible to immune attack or in improving drug efficacy. It should also be possible to use MVs or exosomes isolated directly from the pathogens, or from the cells infected with pathogens, to provide alternative vaccination strategies.


2021 ◽  
Vol 124 ◽  
pp. 105064
Author(s):  
Lulu Li ◽  
Beibei Cong ◽  
Xixi Yu ◽  
Songsong Deng ◽  
Mengjia Liu ◽  
...  

1990 ◽  
Vol 7 (2) ◽  
pp. 78-89 ◽  
Author(s):  
Tsukasa Seya ◽  
Tomoko Hara ◽  
Akiko Uenaka ◽  
Eiichi Nakayama ◽  
Hitoshi Akedo

Vox Sanguinis ◽  
1996 ◽  
Vol 71 (4) ◽  
pp. 243-244
Author(s):  
Yasuo Fukumori ◽  
Tsukasa Seya ◽  
Shiro Ohnoki ◽  
Hirotoshi Shibata ◽  
Hideo Yamaguchi

2012 ◽  
Vol 61 (1) ◽  
pp. 84-94 ◽  
Author(s):  
Michaela Frolíková ◽  
Romana Stopková ◽  
Jana Antalíková ◽  
Peter M. Johnson ◽  
Pavel Stopka ◽  
...  

Vaccine ◽  
2008 ◽  
Vol 26 ◽  
pp. I75-I78 ◽  
Author(s):  
Maria A. Oliver ◽  
José M. Rojo ◽  
Santiago Rodríguez de Córdoba ◽  
Sebastián Alberti

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