User:Marvin O'Neal/VlsE: Difference between revisions

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VlsE is essential to the persistence and virulence of Lyme disease and is upregulated under humoral immune pressure.<ref name="G">PMID:17714442</ref> <ref name="H">PMID:15385475</ref>  While the exact mechanism for immune evasion remains unknown several theories have been put forth.  One popular theory maintains that VlsE masks other surface antigens by coating the surface of the bacteria, thereby sterically blocking the antigens from antibody binding.  This is similar to other pathogens with variable regions, such as the [http://en.wikipedia.org/wiki/Trypanosoma_brucei protozoa] responsible for African sleeping sickness and also the [http://en.wikipedia.org/wiki/Neisseria_gonorrhoeae bacterium] that causes gonorrhea.  However, recent studies have cast doubt on this theory.  An alternate theory provides that VlsE directly stimulates B cell antibody production independent of T-cells.  The robust response elicited is thought to override antibody production against other antigens.<ref name="G" />   
VlsE is essential to the persistence and virulence of Lyme disease and is upregulated under humoral immune pressure.<ref name="G">PMID:17714442</ref> <ref name="H">PMID:15385475</ref>  While the exact mechanism for immune evasion remains unknown, several theories have been put forth.  One popular theory maintains that VlsE masks other surface antigens by coating the surface of the bacteria, thereby sterically blocking the antigens from antibody binding.  This is similar to other pathogens with variable regions, such as the [http://en.wikipedia.org/wiki/Trypanosoma_brucei protozoa] responsible for African sleeping sickness and also the [http://en.wikipedia.org/wiki/Neisseria_gonorrhoeae bacterium] that causes gonorrhea.  However, recent studies have cast doubt on this theory.  An alternate theory provides that VlsE directly stimulates B cell antibody production independent of T-cells.  The robust response elicited is thought to override antibody production against other antigens.<ref name="G" />   
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