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IL17a - Undo Autism?

roller

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Researchers injected mice with an acid that mimics a viral infection. This caused the pregnant mice's immune system to produce a chemical called IL-17a.

Mice exposed to higher IL-17a levels in the womb exhibited autism-like symptoms when they were born.

For example, they had trouble telling the difference between another live mouse and a toy.
They interacted with both equally, whereas normal mice spent more time socially interacting with live mice.

Yet, blocking the action of Th17 cells completely restored normal structure and function to the brains of the study offspring.

This was regardless of whether the changes were achieved by treatment with antibodies or by shutting down the IL-17a gene.

'To our knowledge, this is the first study to identify a specific population of immune cells that may have a direct role in causing behaviors linked to autism,' said immunologist study author Dan Littman at NYU Langone.

Read more:http://www.dailymail.co.uk/sciencetech/article-3421329/Have-scientists-cure-autism-Blocking-specific-cells-pregnancy-help-prevent-disorder-developing.html
 

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RESEARCH ARTICLE
The maternal interleukin-17a pathway in mice promotes autismlike phenotypes in offspring

†Corresponding author. E-mail:charles.hoeffer@colorado.edu(C.A.H.);dan.littman@med.nyu.edu(D.R.L.);jun.huh@umassmed.edu(J.R.H.) .*These authors contributed equally to this work

Science 28 Jan 2016: pp.
DOI: 10.1126/science.aad0314


"Viral infection during pregnancy has been correlated with increased frequency of autism spectrum disorder (ASD) in offspring. This observation has been modeled in rodents subjected to maternal immune activation (MIA). The immune cell populations critical in the MIA model have not been identified. Using both genetic mutants and blocking antibodies in mice, we show that retinoic acid receptor–related orphan nuclear receptor γt (RORγt)–dependent effector T lymphocytes [e.g., T helper 17 (TH17) cells] and the effector cytokine interleukin-17a (IL-17a) are required in mothers for MIA-induced behavioral abnormalities in offspring. We find that MIA induces an abnormal cortical phenotype, which is also dependent on maternal IL-17a, in the fetal brain. Our data suggest that therapeutic targeting of TH17 cells in susceptible pregnant mothers may reduce the likelihood of bearing children with inflammation-induced ASD-like phenotypes."

http://science.sciencemag.org/content/early/2016/01/28/science.aad0314.full
 

adreno

PR activist
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Note that this was used to prevent autism-like phenotypes in offspring, not as a cure for those already born.
 

natasa778

Senior Member
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1,774
I think I just read that baicalin works on th17.

interesting, thank you!

Ba reduced infiltration of immune cells into the CNS, inhibited expression of proinflammatory molecules and chemokines, and prevented Th1 and Th17 cell differentiation via STAT/NFκB signaling pathways. Further, we showed that SOCS3 induction is essential to the effects of Ba, given that the inhibitory effect of Ba on pathogenic Th17 responses was largely abolished when SOCS3 signaling was knocked down. Taken together, our findings demonstrate that Ba has significant potential as a novel anti-inflammatory agent for therapy of autoimmune diseases such as MS.
...

http://www.nature.com/articles/srep17407