Lyme, LYMErix and the Plague (TLR2/CD14 and Immunosuppression) [I AM LMAO !!]
Kathleen
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Subject: Lyme, LYMErix and the Plague (TLR2/CD14 and
Immunosuppression)
Date: Jan 12, 2011 8:48 AM
"The ability of LcrV to utilize human IFN-gamma (a major inflammatory
effector of innate immunity) to minimize inflammation is insidious and
may account in part for the severe symptoms of plague in man." --
RUSSIA
http://www.ncbi.nlm.nih.gov/pubmed/17441749
========================
Yep.
The immunosuppression caused by
LYMErix-like antigens and their
ability to activate other viral
and mycoplasma/fungal infections,
http://www.actionlyme.org/101016.htm
could be involved in the catastrophic
effects of illnesses like plague, which
means LYMErix was never a vaccine, which
means the "results" of its "safety and
efficacy" were falsified.
AND, like I told the HomeLames
5.5 years ago:
http://www.actionlyme.org/LYME_CORRUPTICUT.htm
if we continue to rely on antibody
testing, other nations' bioweapons
programs will get the best of us.
:)))
And they have (China & Russia).
:)))
http://www.ncbi.nlm.nih.gov/pubmed/14617145
"Although the spirochetal protein OspA is capable of stimulating
immune cells in a CD14- and TLR2-dependent manner, little is known
about how TLR2 receptor complex ligands, such as OspA, are handled by
the cell once delivered."
And:
http://www.ncbi.nlm.nih.gov/pubmed/10452971
"Futhermore, TLR2-dependent signaling by lipoproteins was facilitated
by CD14."
http://www.ncbi.nlm.nih.gov/pubmed/17441749
Abstract
The virulence antigen (V-antigen, LcrV) of Yersinia pestis, the
causative agent of bubonic plague, is an established protective
antigen known to regulate, target, and mediate type III translocation
of cytotoxic yersiniae outer proteins termed Yops; LcrV also prompts
TLR2-dependent upregulation of anti-inflammatory IL-10. In this study,
we determined the parameters of specific interaction of LcrV with TLR2
expressed on human transfected HEK293 cells (TLR2+/CD14-), VTEC2.HS
cells (TLR2+/CD14-), primary monocytes (TLR2+/CD14+), and THP-1 cells
(TLR2+/CD14+). The IRRL314-317 motif of the extracellular domain of
human and mouse TLR2 accounted for high-affinity binding of LcrV. The
CD14 co-receptor did not influence this interaction. LcrV did not bind
to human U937 (TLR2-/CD14-) and alveolar macrophages (TLR2-/CD14+) in
the absence of receptor-bound human IFN-gamma or a synthetic C-
terminal fragment (hIFN-gamma132-143). The latter, but not mouse IFN-
gamma (or synthetic control peptides), shared a GRRA138-141 site
necessary for high-affinity specific binding. LcrV of Y. pestis shares
the N-terminal LEEL32-35 binding site of Yersinia enterocolitica and
also has an exposed internal DEEI203-206 binding site. Comparison of
binding constants and consideration of steric restrictions indicate
that binding is not cooperative and only the internal site binds LcrV
to target cells. Both the LEEL32-35 and DEEI203-206 binding sites are
removed by five amino acids from DKN residues associated with
biological activity of bound LcrV. LcrV of Y. pestis promoted both
TLR2/CD14-dependent and TLR2/CD14-independent amplification of IL-10
and concomitant downregulation of TNF-alpha in human target cells. The
ability of LcrV to utilize human IFN-gamma (a major inflammatory
effector of innate immunity) to minimize inflammation is insidious and
may account in part for the severe symptoms of plague in man.
============
Laughing my *ss off...
KMDickson