NYU Disagrees with Arthur Weinstein and Agrees with Team C (ActionLyme/LymeCryme)
Mort Zuckerman
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Subject: NYU Disagrees with Arthur Weinstein and Agrees with Team C
(ActionLyme/LymeCryme)
Date: Sep 22, 2009 10:15 AM
NYU scientific journal article on how OspA or
the Lyme vaccines suppress the immune system below
==================
============================
Team C says OspA causes immunosuppression:
http://www.actionlyme.org/Pam3Cys_Version15.htm
Weinstein says, "Lyme is either inflammatory or it's
imaginary."
http://www.actionlyme.org/index.htm
(Use your browser to search for his name, and
where his topic starts- and it is a very long topic..)
NYU (below) says Lyme and OspA vaccination cause
immunosuppression through various mechanisms, not least of
which, mentioned in the Pam3Cys presentation (Justin Radolf),
is the reduction of MHC Class II molecules, resulting in NO
ANTIBODIES BEING PRODUCED which contrasts greatly
with Weinstein's "validation" of Steere's proposal that "The More
Antibodies, The More Valid-er:"
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=8053960[uid]
That ^^ is a real winner, lemme tellya. (Don't take this bull
to a china shop, if ya know what I mean. If ya take him
playing golf, giving him a 400 handicap. This boy needs
tractor treads on his skateboard...)
And here is NYU, saying everything *WE* said, Thank you:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=19629181
Mycobacterium tuberculosis uses multiple mechanisms to avoid
elimination by the immune system. We have previously shown that M.
tuberculosis can inhibit selected macrophage responses to IFN-γ
through TLR2-dependent and -independent mechanisms. To specifically
address the role of TLR2 signaling in mediating this inhibition, we
stimulated macrophages with the specific TLR2/1 ligand ***Pam3CSK4 and
assayed responses to IFN-γ. Pam3CSK4 stimulation prior to IFN-γ
inhibited transcription of the unrelated IFN-γ-inducible genes, CIITA
and CXCL11. Surface expression of MHC class II and secretion of CXCL11
were greatly reduced as well,*** indicating that the reduction in
transcripts had downstream effects. Inhibition of both genes required
new protein synthesis. Using chromatin immunoprecipitation, we found
that TLR2 stimulation inhibited IFN-γ-induced RNA polymerase II
binding to the CIITA and CXCL11 promoters. Furthermore, TATA binding
protein was unable to bind the TATA box of the CXCL11 promoter,
suggesting that assembly of transcriptional machinery was disrupted.
However, TLR2 stimulation affected chromatin modifications differently
at each of the inhibited promoters. Histone H3 and H4 acetylation was
reduced at the CIITA promoter but unaffected at the CXCL11 promoter.
In addition, NF-κB signaling was required for inhibition of CXCL11
transcription, but not for inhibition of CIITA. Taken together, these
results indicate that TLR2-dependent inhibition of IFN-γ-induced gene
expression is mediated by distinct, gene-specific mechanisms that
disrupt binding of the transcriptional machinery to the promoters."
Kathleen M. Dickson
"Dangerously Intelligent" "Chemist"
of America, USA And Make Good
Researches To! For Most Glorious
Country... :)))
http://www.actionlyme.org
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci