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Update to research papers


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Hi folks, just a comment that I've updated the research papers to include some recent papers by Wang and Cleary in 2010. http://www.latitudes.org/forums/index.php?showtopic=5144&st=0&p=36300entry36300

 

 

 

Th17, Autoimmunity and the blood brain barrier

 

 

Recently, Wang et al published a remarkable finding that repeated nasal innoculation with live (or dead) GABHS produced Th17 cell response in mice. Th17 was recently identified in 2006 (see Annunziato et al ) and is highly implicated in auto-immune disorders.

 

In 2007, Kebir et al published the paper "Human TH17 lymphocytes promote blood-brain barrier disruption and central nervous system inflammation" where it was shown that these Th17 cells are highly pro-inflammatory and promote blood-brain barrier disruption. Perhaps this is the missing link in how auto-antibodies are crossing the blood brain barrier (i.e., GABHS carriage triggers Th17, GABHS infection triggers anti-neuronal antibodies, Th17 disrupts the BBB allowing anti-neuronal antibodies (or B/T-cells) to cross). I certainly hope more research is done here.

 

While this is a mouse model and may not apply to humans, the study is noteworthy because only carriage was needed. This may explain why an apparent "allergic" reaction is seen in some children -- i.e., that only colonization is necessary on subsequent exposure and not infection.

 

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Hi folks, just a comment that I've updated the research papers to include some recent papers by Wang and Cleary in 2010. http://www.latitudes.org/forums/index.php?showtopic=5144&st=0&p=36300entry36300

 

 

 

Th17, Autoimmunity and the blood brain barrier

 

 

Recently, Wang et al published a remarkable finding that repeated nasal innoculation with live (or dead) GABHS produced Th17 cell response in mice. Th17 was recently identified in 2006 (see Annunziato et al ) and is highly implicated in auto-immune disorders.

 

In 2007, Kebir et al published the paper "Human TH17 lymphocytes promote blood-brain barrier disruption and central nervous system inflammation" where it was shown that these Th17 cells are highly pro-inflammatory and promote blood-brain barrier disruption. Perhaps this is the missing link in how auto-antibodies are crossing the blood brain barrier (i.e., GABHS carriage triggers Th17, GABHS infection triggers anti-neuronal antibodies, Th17 disrupts the BBB allowing anti-neuronal antibodies (or B/T-cells) to cross). I certainly hope more research is done here.

 

While this is a mouse model and may not apply to humans, the study is noteworthy because only carriage was needed. This may explain why an apparent "allergic" reaction is seen in some children -- i.e., that only colonization is necessary on subsequent exposure and not infection.

 

 

Thank You...as always!!!

 

PS thanks dawn, i like how the link you posted talks about gut and how it reacts with the brain!!

Edited by Fixit
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