Monkey TLR2s and the Revenge of the Penis-Ports
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Mort Zuckerman
Aug 14, 2008, 7:07:05 PM8/14/08
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Subject: Monkey TLR2
Date: Aug 14, 2008 7:04 PM
Uh, a little slow on the pick-up, here. Tolerance to TLR2-ticklers
results immune suppression. Because Borrelia constantly shed these
antigens, a Lyme infected person is autovaccinated every day with
the same goob. This is what "chronic Lyme" is. It is all the immune
suppression outcomes of TLR2 tolerization.
============================
http://www.ncbi.nlm.nih.gov/pubmed/18694963?ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Infect Immun. 2008 Aug 11. [Epub ahead of print]Click here to read
Links
TOLL-LIKE RECEPTORS: INSIGHTS INTO THEIR POSSIBLE ROLE IN THE
PATHOGENESIS OF
LYME NEUROBORRELIOSIS.
Bernardino AL, Myers TA, Alvarez X, Hasegawa A, Philipp MT.
Divisions of Bacteriology and Parasitology, Comparative Pathology,
and Immunology,
Tulane National Primate Research Center, Tulane University, Covington,
LA.
Lyme neuroborreliosis is likely caused by inflammatory effects of
the tick-borne
spirochete Borrelia burgdorferi on the nervous system. Microglia, the
resident macrophage
cells within the central nervous system (CNS), are important in
initiating an immune
response to microbial products. In addition, astrocytes, the major CNS
glial cell
type, also can contribute to brain inflammation. TLRs (Toll-Like
Receptors) are
used by glial cells to recognize pathogen-associated molecular
patterns (PAMPs),
mediate innate responses, and initiate an acquired immune response.
Here we hypothesize
that because of their PAMP specificities, TLR 1, 2, 5, and 9 may be
involved in
the pathogenesis of Lyme neuroborreliosis. Previous reports have shown
that the
rhesus monkey is the only animal model to exhibit signs of Lyme
neuroborreliosis.
Therefore, we used primary cultures of rhesus astrocytes and microglia
to determine
the role of TLRs in mediating pro-inflammatory responses to B.
burgdorferi. The
results indicate that microglia and astrocytes respond to B.
burgdorferi through
TLR1/2 and TLR5. In addition, we observed that phagocytosis of B.
burgdorferi by
microglia enhances not only the expression of TLR1, 2, and 5, but also
that of TLR4.
Taken together, our data provide proof of the concept that astrocyte
and microglial
TLR 1, 2, and 5 are involved in the in vivo response of primate glial
cells to B.
burgdorferi. The pro-inflammatory molecules elicited by these TLR-
mediated responses
could be a significant factor in the pathogenesis of Lyme
neuroborreliosis.
=============
http://www.actionlyme.org/SCIENTIST_VS_LUNATIC.htm
http://www.jimmunol.org/cgi/content/full/173/4/2660
The Journal of Immunology, 2004, 173: 2660-2668.
Copyright © 2004 by The American Association of Immunologists
Mycobacterium tuberculosis LprG (Rv1411c): A Novel TLR-2 Ligand That
Inhibits Human
Macrophage Class II MHC Antigen Processing1
"Signaling through TLR-2 by lipoproteins may represent a double-edged
sword
for host responses to chronic intracellular pathogens such as M.
tuberculosis. Short-term
signaling through TLR-2 activates macrophages and initiates acute
inflammation that
may help control initial infection. In contrast, prolonged TLR-2
signaling in macrophages
results in down-regulation of certain critical immune functions, such
as MHC-II
Ag processing. M. tuberculosis infects, survives, and persists in
macrophages. The
ability of M. tuberculosis to survive acute inflammation positions the
bacilli to
take advantage, through secretion of lipoproteins such as LprG and
LpqH, of this
down-regulation of macrophage immune function."
===========
http://www.actionlyme.org/Duray.htm
"On occasion, these atypical-appearing large lymphocytes have been
misinterpreted
in biopsy by several laboratories as cells of a malignant lymphoma or
leukemia.
Bb antigens, then, may stimulate growth of immature lymphocytic
suibsets in some
target organs, as well as in the cerebrospinal fluid (Szyfelbein and
Ross 1988).
Usual bacterial infections do not produce such lymphocytic infiltrates
in tissue.
These immunoblastoid cells in Bb infections at times resemble those
found in Epstein-Barr
virus infections. Does Bb reactivate latent virus infections in
tissues? Do some
tick inocula harbor simultaneous infectious agents (ixodid ticks can
harbor Rickettsiae,
Babesia microti, and Ehrlichia bacteria, in addition to Bb), producing
multi-agent
infections in some hosts? Further studies can clarify these issues by
mans of tissue-based
molecular probe analysis." - Paul Duray, NCI, NIH, Ft. Detrick, at
the 1992
Cold Spring Harbor Crooks' Conference, published in Steve Schutzer's
Lyme
Disease: Molecular and Immunologic Approaches.
http://www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770/ref=sr_1_2?ie=UTF8&s=books&qid=1214848669&sr=1-2
=========================
Pam3Cys (it may be Pam2Cys) activates HIV replication:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15312143
Immunology. 2004 September; 113(1): 121–129.
Copyright © 2004 Blackwell Publishing Ltd
Lipid-associated membrane proteins of Mycoplasma fermentans and M.
penetrans activate
human immunodeficiency virus long-terminal repeats through Toll-like
receptors
Mycoplasmas are known to enhance human immunodeficiency virus (HIV)
replication,
and mycoplasma-derived lipid extracts have been reported to activate
nuclear factor-κB
(NF-κB) through Toll-like receptors (TLRs). In this study, we examined
the involvement
of TLRs in the activation of HIV long-terminal repeats (LTR) by
mycoplasma and their
active components responsible for the TLR activation. Lipid-associated
membrane
proteins (LAMPs) from two species of mycoplasma (Mycoplasma fermentans
and M. penetrans)
that are associated with acquired immune-deficiency syndrome (AIDS),
were found
to activate HIV LTRs in a human monocytic cell line, THP-1. NF-κB
deletion from
the LTR resulted in inhibition of the activation. The LTR activation
by M. fermentans
LAMPs was inhibited by a dominant negative (DN) construct of TLR1 and
TLR6, whereas
HIV LTR activation by M. penetrans LAMPs was inhibited by DN TLR1, but
not by DN
TLR6. These results indicate that the activation of HIV LTRs by M.
fermentans and
M. penetrans LAMPs is dependent on NF-κB, and that the activation of
HIV LTR by
M. fermentans LAMPs is mediated through TLR1, TLR2 and TLR6. In
contrast, the LTR
activation by M. penetrans LAMPs is carried out through TLR1 and TLR2,
but not TLR6.
Subsequently, the active component of M. penetrans and M. fermentans
LAMPs was purified
by reverse-phase high-performance liquid chromatography (HPLC).
Interestingly, the
purified lipoprotein of M. penetrans LAMPs (LPMp) was able to activate
NF-κB through
TLR1 and TLR2. On the other hand, the activation of NF-κB by purified
lipoprotein
of M. fermentans LAMPs (LPMf) was mediated through TLR2 and TLR6, but
not TLR1.
===========================
We looked into the matter of whether or not the Lyme criminals had
actually published
anything that really proved they had a vaccine. We found numerous
reports that
showed this vaccine failed in animal studies.
http://www.actionlyme.org/FUNGAL_VACCINES.htm
And:
"Accordingly, the methods of the invention provide a powerful and
selective
approach for modulating the innate immune response pathways in animals
without giving
rise to the toxicities often associated with the native bacterial
components that
normally stimulate those pathways."
http://patft.uspto.gov/6,800,613
"Although a single ligation of TLRs induces responses such as TNF
production,
repeated ligation will lead to a loss of response, i.e., the cells
become tolerant."
http://www.jimmunol.org/cgi/content/full/173/4/2736
"Borrelia burgdorferi-Induced Tolerance as a Model of Persistence via
Immunosuppression"
- "In summary, we characterized tolerance induced by B. burgdorferi,
describing
a model of desensitization which might mirror the immunosuppression
recently attributed
to the persistence of Borrelia in immunocompetent hosts."
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12819085
http://www.ncbi.nlm.nih.gov/pubmed/16889623?ordinalpos=8&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Cell Microbiol. 2007 Jan;9(1):142-53. Epub 2006 Aug 2.Click here to
read Links
The inhibitory effect of Mycoplasma fermentans on tumour necrosis
factor (TNF)-alpha-induced
apoptosis resides in the membrane lipoproteins.
Gerlic M, Horowitz J, Farkash S, Horowitz S.
Department of Microbiology and Immunology, Faculty of Health
Sciences, Soroka
University Medical Center, Ben-Gurion University of the Negev,
Beer-Sheva, Israel,
84105.
Mycoplasma have been shown to be involved in the alteration of
several eukaryotic
cell functions, such as cytokine production, gene expression and
more. We have
previously
reported that infection of human myelomonocytic U937 cell line
with live Mycoplasma
fermentans (M. fermentans) inhibited tumour necrosis factor (TNF-
alpha)-induced
apoptosis. Mycoplasmal membrane lipoproteins are considered to be
the most potent
initiators of inflammatory reactions in mycoplasmal infections.
The aim of this
study was to clarify whether the inhibitory effect on TNFalpha-
induced apoptosis
is exerted by M. fermentans lipoproteins (LPMf). A significant
reduction in
TNFalpha-induced
apoptosis was demonstrated by stimulation of U937 cells with M.
fermentans total
proteins, LPMf or MALP-2 (M. fermentans synthetic lipopeptide),
but not with
M.
fermentans hydrophilic protein preparation (AqMf). ***To
investigate the mechanism
of M. fermentans antiapoptotic effect, the reduction of
mitochondrial transmembrane
potential (delta psi m) was measured. M. fermentans total proteins
LPMf and
MALP-2,
but not AqMf, inhibited the reduction of delta psi m. In addition,
M. fermentans
total proteins LPMf and MALP-2, but not AqMf, downregulated the
formation of
active
caspase-8.*** NF-kappaB was transactivated in cells treated with
M. fermentans
lipoproteins, and was essential for host cell survival, but not
for the inhibition
of TNFalpha-induced apoptosis by LPMf. *** Our results suggest
that the inhibitory
effect exerted by M. fermentans on TNFalpha-induced apoptosis in
U937 cells
is due
to the membrane lipoproteins of these bacteria.***
==================
More from FUNGAL VACCINES:
A) http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10792376&dopt=Abstract
The 19-kD antigen and protective immunity in a murine model of
tuberculosis.
Yeremeev VV, Lyadova IV, Nikonenko BV, Apt AS, Abou-Zeid C, Inwald J,
Young DB.
"The 19-kD antigen is a cell wall-associated lipoprotein present
in Mycobacterium
tuberculosis and in bacille Calmette-Guérin (BCG) vaccine strains.
Expression of
the 19-kD antigen as a recombinant protein in two saprophytic
mycobacteria-M. vaccae
and M. smegmatis-resulted in abrogation of their ability to confer
protection against
M. tuberculosis in a murine challenge model, and in their ability to
prime a DTH
response to cross-reactive mycobacterial antigens. Induction of an
immune response
to the 19-kD antigen by an alternative approach of DNA vaccination had
no effect
on subsequent M. tuberculosis challenge. These results are consistent
with a model
in which the presence of the 19-kD protein has a detrimental effect on
the efficacy
of vaccination with live mycobacteria. Targeted inactivation of genes
encoding selected
antigens represents a potential route towards development of improved
vaccine candidates."
B) http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11179309&dopt=Abstract
Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits
Mycobacterium smegmatis-induced
cytokine production by human macrophages in vitro.
Post FA, Manca C, Neyrolles O, Ryffel B, Young DB, Kaplan G.
Vaccination of mice with Mycobacterium vaccae or M. smegmatis
induces some protection
against M. tuberculosis challenge. The 19-kDa lipoprotein of M.
tuberculosis, expressed
in M. vaccae or M. smegmatis (M. smeg19kDa), abrogates this protective
immunity.
To investigate the mechanism of this suppression of immunity, human
monocyte-derived
macrophages (MDM) were infected with M. smeg19kDa. Infection resulted
in reduced
production of tumor necrosis factor alpha (TNF-alpha) (P < 0.01),
interleukin-12
(IL-12) (P < 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared
to
infection with M. smegmatis vector (M. smegV). Infection with M.
smeg19kDa and with
M. smegV had no differential effect on expression of costimulatory
molecules on
MDM, nor did it affect the proliferation of presensitized T cells
cocultured with
infected MDM. When MDM were infected with M. smegmatis expressing
mutated forms
of the 19-kDa lipoprotein, including non-O-glycosylated (M.
smeg19NOG), nonsecreted
(M. smeg19NS), and nonacylated (M. smeg19NA) variants, the reduced
production of
TNF-alpha or IL-12 was not observed. When the purified 19-kDa
lipoprotein was added
directly to cultures of infected monocytes, there was little effect on
either induction
of cytokine production or its inhibition. Thus, the immunosuppressive
effect is
dependent on glycosylated and acylated 19-kDa lipoprotein present in
the phagosome
containing the mycobacterium. These results suggest that the
diminished protection
against challenge with M. tuberculosis seen in mice vaccinated with M.
smegmatis
expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha
and IL-12 production,
possibly leading to reduced induction of T-cell activation."
C) http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12761093
Infect Immun. 2003 Jun;71(6):3146-54. Related Articles, Links
The Mycobacterium tuberculosis recombinant 27-kilodalton
lipoprotein induces
a strong Th1-type immune response deleterious to protection.
Hovav AH, Mullerad J, Davidovitch L, Fishman Y, Bigi F, Cataldi A,
Bercovier
H.
Department of Clinical Microbiology, Faculty of Medicine, The
Hebrew University,
Jerusalem, Israel.
Th1 immune response is essential in the protection against
mycobacterial intracellular
pathogens. Lipoproteins trigger both humoral and cellular immune
responses and may
be candidate protective antigens. We studied in BALB/c mice the
immunogenicity and
the protection offered by the recombinant 27-kDa Mycobacterium
tuberculosis lipoprotein
and the corresponding DNA vaccine. Immunization with the 27-kDa
antigen resulted
in high titers of immunoglobulin G1 (IgG1) and IgG2a with a typical
Th1 profile
and a strong delayed hypersensitivity response. A strong proliferation
response
was observed in splenocytes, and significant nitric oxide production
and gamma interferon
secretion but not interleukin 10 secretion were measured. Based on
these criteria,
the 27-kDa antigen induced a typical Th1-type immune response thought
to be necessary
for protection. Surprisingly, in 27-kDa-vaccinated mice (protein or
DNA vaccines)
challenged by M. tuberculosis H37Rv or BCG strains, there was a
significant increase
in the numbers of CFU in the spleen compared to that for control
groups. Furthermore,
the protection provided by BCG or other mycobacterial antigens was
completely abolished
once the 27-kDa antigen was added to the vaccine preparations. This
study indicates
that the 27-kDa antigen has an adverse effect on the protection
afforded by recognized
vaccines. We are currently studying how the 27-kDa antigen modulates
the mouse immune
response.
=====================
The first record that we can find on the OspA kind of antigen:
1983: Synthesis of the mitogenic S-[2,3-bis(palmitoyloxy)propyl]-N-
palmitoylpentapeptide
from Escherichia coli lipoprotein.
http://www.ncbi.nlm.nih.gov/pubmed/6347861?ordinalpos=131&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Several reports which make it appear as if the Pam3Cys type of antigen
was used
as an HIV vaccine adjuvant or is actually part of the HIV gp120 and
gp41 (I cannot
find out officially):
1) http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1421990&blobtype=pdf
2) http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=1349173
3) http://www.ncbi.nlm.nih.gov/pubmed/18524817?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
We found decreased Toll-like receptor 1 (TLR1) and TLR4 surface
expression in
HIV-infected U1 monocytic cells compared to the uninfected parental
U937 cell line
and decreased TLR message in alveolar macrophages (AMs) from HIV-
positive subjects.
In addition, stimulation with TLR1/2 ligand (Pam(3)Cys) or TLR4 ligand
(lipopolysaccharide)
resulted in decreased intracellular phosphorylated extracellular
signal-regulated
kinase and subsequent decreased transcription and expression of TNF-
alpha in U1
cells compared to U937 cells.
4) http://journal.kcsnet.or.kr/main/j_search/j_download.htm?code=B961118
(Korean
Journal where they blew up this HIV-Pam3Cys thing to look for
“We are currently using several mass spectral techniques to
characterize the
amino acid sequences of the Pam3Cys peptides found in the envelop
glycoproteins
of the HIV-1 and the Simian Immunodeficiency Virus (SIV).(17)
Convential FAB-MS
analysis using standard matrices, such as glycerol and nitrobenzyl
alcohol, is not
particularly effective for these molecules, largely due to their
tendency to aggregate”
[“their tendency to aggregate” …like what happened with LYMErix and
the Western
blot smudging, we think. We think they could never guarantee
completely free OspA
antigens in a vial of vaccine, and previous reports about HPLC assay
of OspA, I
suspect had a –prefiltering and pre-HPLC step because we always knew
OspA was a
sticky lipid and even sticks to itself, since Alan Barbour reported
that phenomenon.]
=====================
http://www.ncbi.nlm.nih.gov/pubmed/18162176?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Biochem Biophys Res Commun. 2008 Feb 29;367(1):41-6. Epub 2007 Dec
26. Links
The Ixodes scapularis salivary protein, salp15, prevents the
association of HIV-1
gp120 and CD4.
Juncadella IJ, Garg R, Bates TC, Olivera ER, Anguita J.
Department of Veterinary and Animal Sciences, University of
Massachusetts Amherst,
103 Paige Laboratory, 161 Holdsworth Way, Amherst, MA 01003, USA.
Ixodes scapularis salivary protein, Salp15, inhibits CD4(+) T cell
activation by
binding to the most-extracellular domains of the CD4 molecule,
potentially overlapping
with the gp120-binding region. We now show that Salp15 inhibits the
interaction
of gp120 and CD4. Furthermore, Salp15 prevents syncytia formation
between HL2/3
(a stable HeLa cell line expressing the envelope protein) and CD4-
expressing cells.
Salp15 prevented gp120-CD4 interaction at least partially through its
direct interaction
with the envelope glycoprotein. A phage display library screen
provided the interacting
residues in the C1 domain of gp120. These results provide a potential
basis to define
exposed gp120 epitopes for the generation of neutralizing vaccines.
https://www.aidsreagent.org/program_info.cfm#5
=======================
ON MEDLINE, searching for Pam3Cys and HIV or tripalmitoyl and HIV:
: J Virol Methods. 1988 Dec;22(2-3):173-82.Links
Distinction between HIV-1 and HIV-2 infection using novel synthetic
lipopeptide
conjugates as antigens in enzyme immunoassays.
Böltz T, Hummel RP, Tröger W, Rübsamen-Waigmann H, Biesert L, Müller-
Lantzsch N,
Koch P, Bessler W, Jung G.
Institut für Immunobiologie, Universität Freiburg, F.R.G.
A novel immunoassay technique using synthetic lipopeptide (Pam3Cys-
Ser) linked to
immunodominant peptide domains of HIV-1 and HIV-2 envelope proteins as
an antigen
adsorbent has been developed. Attachment of peptides to microtiter
plates can be
considerably improved with this method by employing the hydrophobic
properties of
lipopeptide. From the sera of 121 HIV-1 infected patients 117 reacted
with Pam3Cys-Ser-[HIV-1(598-609)cyclic
disulfide]. Five of 5 HIV-2 positive sera were positive with Pam3Cys-
Ser-[HIV-2(593-603)cyclic
disulfide]. Control sera failed to react with these conjugate
==================
Now, none of this will be in Pam Weintraub's book because I had
not published it all in one place before, except for the first page
I put up on what was wrong with LYMErix in 2003, and of course I
mentioned it to the FDA Vaccine Committee in 2001:
http://www.actionlyme.org/DICKSON_FDA_TEXT.htm
"OUTLOOK
"By what mechanism vaccination of the asymptomatic Bb infected
patients
is causing the Lyme like illness, we do not know exactly.
"Previous infection could be "priming" the immune system, as Denise
Huber
of Tufts has suggested, in "Identification of LFA-1 as a Candidate
Autoantigen in Treatment-Resistent Lyme Arthritis" July 31, 1998,
Science, Vol 281, p 703.
"or the vaccine is activating a dormant infection by the immune
dysregulation it causes, as demonstrated by the effect of Bb
infection and Osp A alone, on NK cells population, T cells,
neutrophils, and the effects on the various inflammatory
regulating biomoleclues, such as IL-10.
====================================================
The point and the fact is that the crooks were told about this in
1992 at the Cold Spring Harbor conference by Paul Duray in 1992
and probably earlier than that, in the 1989 IDSA Reviews:
http://www.actionlyme.org/Duray.htm
http://www.actionlyme.org/COLDSPRINGHARBOR.htm
and they all knew about it, since Dattwyler, Steere
Klempner and Wormser all reported about it from 1994
onward:
http://www.actionlyme.org/andersonpenisbiter.htm
(Everyone will have to read the DCF penis-biter report in order
to find the links)
THE CROOKS ALL KNEW THAT PEOPLE WHO HAD LOW ANTIBODY
CONCENTRATION WERE THE SICKEST, AND THEY ALL REPORTED THAT.
Lyme is not an inflammatory disease:
http://www.actionlyme.org/CRYMEDISEASE_CHP3_B.htm
This is a crime. The biggest one after 9/11:
http://www.actionlyme.org/070426.htm
Are we going to charge it as crime? or are we going to
hear about how Lyme causes sex, I mean sex causes Lyme
I mean providing orgasms for other people cures alcoholism,
or solar flares are cured by Simon Wessely's Questionaires
or eye of newt and wing of bat or we wimmins put a hex on
thems African sea birds so they'd fly to Long Guy-Land instead
of Miami on thems hurricanes or however Yale's psychiatric
whoring or blame-the-penis-ports (us'n wimmins) stories go...
Whoever figures out either Yale or psychiatry, wins.
Kathleen M. Dickson
http://www.actionlyme.org
kshe...@calea.org, fit...@gmail.com, patrick.f...@usdoj.gov,
model...@sbcglobal.net, jdr...@nejm.org, let...@courant.com,
Jgerb...@cdc.gov, michae...@po.state.ct.us,
con...@po.state.ct.us, executiv...@nytimes.com, managing-
edi...@nytimes.com, news...@nytimes.com, the-...@nytimes.com,
biz...@nytimes.com, for...@nytimes.com, me...@nytimes.com,
nati...@nytimes.com, dv...@cdc.gov, brigidc...@optonline.net,
tr...@hotmail.com, illino...@aol.com, jle...@courant.com,
tinaj...@yahoo.com, jhorn...@fff.org, thomas...@usdoj.gov,
thoma...@po.state.ct.us, kur...@washpost.com,
georg...@washpost.com, p...@allegorypress.com,
commissi...@po.state.ct.us, FalN...@aol.com,
brans...@comcast.net, vts...@comcast.net, o...@po.state.ct.us,
freet...@charter.net, scott....@po.state.ct.us,
govern...@po.state.ct.us, attorney...@po.state.ct.us,
randall...@usdoj.gov
Cc: fra...@ucia.gov, dr-ahma...@president.ir,
eugener...@washpost.com, hor...@courant.com,
bmi...@newstimes.com, tr...@hotmail.com, rast...@aol.com,
billc...@gmail.com, amcg...@rms-law.com, rjmu...@aol.com,
paulcrai...@yahoo.com, sidney_b...@yahoo.com,
criminal...@usdoj.gov, karla.d...@usdoj.gov,
christophe...@usdoj.gov
Subject: Monkey TLR2
Date: Aug 14, 2008 7:04 PM
Uh, a little slow on the pick-up, here. Tolerance to TLR2-ticklers
results immune suppression. Because Borrelia constantly shed these
antigens, a Lyme infected person is autovaccinated every day with
the same goob. This is what "chronic Lyme" is. It is all the immune
suppression outcomes of TLR2 tolerization.
============================
http://www.ncbi.nlm.nih.gov/pubmed/18694963?ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Infect Immun. 2008 Aug 11. [Epub ahead of print]Click here to read
Links
TOLL-LIKE RECEPTORS: INSIGHTS INTO THEIR POSSIBLE ROLE IN THE
PATHOGENESIS OF
LYME NEUROBORRELIOSIS.
Bernardino AL, Myers TA, Alvarez X, Hasegawa A, Philipp MT.
Divisions of Bacteriology and Parasitology, Comparative Pathology,
and Immunology,
Tulane National Primate Research Center, Tulane University, Covington,
LA.
Lyme neuroborreliosis is likely caused by inflammatory effects of
the tick-borne
spirochete Borrelia burgdorferi on the nervous system. Microglia, the
resident macrophage
cells within the central nervous system (CNS), are important in
initiating an immune
response to microbial products. In addition, astrocytes, the major CNS
glial cell
type, also can contribute to brain inflammation. TLRs (Toll-Like
Receptors) are
used by glial cells to recognize pathogen-associated molecular
patterns (PAMPs),
mediate innate responses, and initiate an acquired immune response.
Here we hypothesize
that because of their PAMP specificities, TLR 1, 2, 5, and 9 may be
involved in
the pathogenesis of Lyme neuroborreliosis. Previous reports have shown
that the
rhesus monkey is the only animal model to exhibit signs of Lyme
neuroborreliosis.
Therefore, we used primary cultures of rhesus astrocytes and microglia
to determine
the role of TLRs in mediating pro-inflammatory responses to B.
burgdorferi. The
results indicate that microglia and astrocytes respond to B.
burgdorferi through
TLR1/2 and TLR5. In addition, we observed that phagocytosis of B.
burgdorferi by
microglia enhances not only the expression of TLR1, 2, and 5, but also
that of TLR4.
Taken together, our data provide proof of the concept that astrocyte
and microglial
TLR 1, 2, and 5 are involved in the in vivo response of primate glial
cells to B.
burgdorferi. The pro-inflammatory molecules elicited by these TLR-
mediated responses
could be a significant factor in the pathogenesis of Lyme
neuroborreliosis.
=============
http://www.actionlyme.org/SCIENTIST_VS_LUNATIC.htm
http://www.jimmunol.org/cgi/content/full/173/4/2660
The Journal of Immunology, 2004, 173: 2660-2668.
Copyright © 2004 by The American Association of Immunologists
Mycobacterium tuberculosis LprG (Rv1411c): A Novel TLR-2 Ligand That
Inhibits Human
Macrophage Class II MHC Antigen Processing1
"Signaling through TLR-2 by lipoproteins may represent a double-edged
sword
for host responses to chronic intracellular pathogens such as M.
tuberculosis. Short-term
signaling through TLR-2 activates macrophages and initiates acute
inflammation that
may help control initial infection. In contrast, prolonged TLR-2
signaling in macrophages
results in down-regulation of certain critical immune functions, such
as MHC-II
Ag processing. M. tuberculosis infects, survives, and persists in
macrophages. The
ability of M. tuberculosis to survive acute inflammation positions the
bacilli to
take advantage, through secretion of lipoproteins such as LprG and
LpqH, of this
down-regulation of macrophage immune function."
===========
http://www.actionlyme.org/Duray.htm
"On occasion, these atypical-appearing large lymphocytes have been
misinterpreted
in biopsy by several laboratories as cells of a malignant lymphoma or
leukemia.
Bb antigens, then, may stimulate growth of immature lymphocytic
suibsets in some
target organs, as well as in the cerebrospinal fluid (Szyfelbein and
Ross 1988).
Usual bacterial infections do not produce such lymphocytic infiltrates
in tissue.
These immunoblastoid cells in Bb infections at times resemble those
found in Epstein-Barr
virus infections. Does Bb reactivate latent virus infections in
tissues? Do some
tick inocula harbor simultaneous infectious agents (ixodid ticks can
harbor Rickettsiae,
Babesia microti, and Ehrlichia bacteria, in addition to Bb), producing
multi-agent
infections in some hosts? Further studies can clarify these issues by
mans of tissue-based
molecular probe analysis." - Paul Duray, NCI, NIH, Ft. Detrick, at
the 1992
Cold Spring Harbor Crooks' Conference, published in Steve Schutzer's
Lyme
Disease: Molecular and Immunologic Approaches.
http://www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770/ref=sr_1_2?ie=UTF8&s=books&qid=1214848669&sr=1-2
=========================
Pam3Cys (it may be Pam2Cys) activates HIV replication:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15312143
Immunology. 2004 September; 113(1): 121–129.
Copyright © 2004 Blackwell Publishing Ltd
Lipid-associated membrane proteins of Mycoplasma fermentans and M.
penetrans activate
human immunodeficiency virus long-terminal repeats through Toll-like
receptors
Mycoplasmas are known to enhance human immunodeficiency virus (HIV)
replication,
and mycoplasma-derived lipid extracts have been reported to activate
nuclear factor-κB
(NF-κB) through Toll-like receptors (TLRs). In this study, we examined
the involvement
of TLRs in the activation of HIV long-terminal repeats (LTR) by
mycoplasma and their
active components responsible for the TLR activation. Lipid-associated
membrane
proteins (LAMPs) from two species of mycoplasma (Mycoplasma fermentans
and M. penetrans)
that are associated with acquired immune-deficiency syndrome (AIDS),
were found
to activate HIV LTRs in a human monocytic cell line, THP-1. NF-κB
deletion from
the LTR resulted in inhibition of the activation. The LTR activation
by M. fermentans
LAMPs was inhibited by a dominant negative (DN) construct of TLR1 and
TLR6, whereas
HIV LTR activation by M. penetrans LAMPs was inhibited by DN TLR1, but
not by DN
TLR6. These results indicate that the activation of HIV LTRs by M.
fermentans and
M. penetrans LAMPs is dependent on NF-κB, and that the activation of
HIV LTR by
M. fermentans LAMPs is mediated through TLR1, TLR2 and TLR6. In
contrast, the LTR
activation by M. penetrans LAMPs is carried out through TLR1 and TLR2,
but not TLR6.
Subsequently, the active component of M. penetrans and M. fermentans
LAMPs was purified
by reverse-phase high-performance liquid chromatography (HPLC).
Interestingly, the
purified lipoprotein of M. penetrans LAMPs (LPMp) was able to activate
NF-κB through
TLR1 and TLR2. On the other hand, the activation of NF-κB by purified
lipoprotein
of M. fermentans LAMPs (LPMf) was mediated through TLR2 and TLR6, but
not TLR1.
===========================
We looked into the matter of whether or not the Lyme criminals had
actually published
anything that really proved they had a vaccine. We found numerous
reports that
showed this vaccine failed in animal studies.
http://www.actionlyme.org/FUNGAL_VACCINES.htm
And:
"Accordingly, the methods of the invention provide a powerful and
selective
approach for modulating the innate immune response pathways in animals
without giving
rise to the toxicities often associated with the native bacterial
components that
normally stimulate those pathways."
http://patft.uspto.gov/6,800,613
"Although a single ligation of TLRs induces responses such as TNF
production,
repeated ligation will lead to a loss of response, i.e., the cells
become tolerant."
http://www.jimmunol.org/cgi/content/full/173/4/2736
"Borrelia burgdorferi-Induced Tolerance as a Model of Persistence via
Immunosuppression"
- "In summary, we characterized tolerance induced by B. burgdorferi,
describing
a model of desensitization which might mirror the immunosuppression
recently attributed
to the persistence of Borrelia in immunocompetent hosts."
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12819085
http://www.ncbi.nlm.nih.gov/pubmed/16889623?ordinalpos=8&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Cell Microbiol. 2007 Jan;9(1):142-53. Epub 2006 Aug 2.Click here to
read Links
The inhibitory effect of Mycoplasma fermentans on tumour necrosis
factor (TNF)-alpha-induced
apoptosis resides in the membrane lipoproteins.
Gerlic M, Horowitz J, Farkash S, Horowitz S.
Department of Microbiology and Immunology, Faculty of Health
Sciences, Soroka
University Medical Center, Ben-Gurion University of the Negev,
Beer-Sheva, Israel,
84105.
Mycoplasma have been shown to be involved in the alteration of
several eukaryotic
cell functions, such as cytokine production, gene expression and
more. We have
previously
reported that infection of human myelomonocytic U937 cell line
with live Mycoplasma
fermentans (M. fermentans) inhibited tumour necrosis factor (TNF-
alpha)-induced
apoptosis. Mycoplasmal membrane lipoproteins are considered to be
the most potent
initiators of inflammatory reactions in mycoplasmal infections.
The aim of this
study was to clarify whether the inhibitory effect on TNFalpha-
induced apoptosis
is exerted by M. fermentans lipoproteins (LPMf). A significant
reduction in
TNFalpha-induced
apoptosis was demonstrated by stimulation of U937 cells with M.
fermentans total
proteins, LPMf or MALP-2 (M. fermentans synthetic lipopeptide),
but not with
M.
fermentans hydrophilic protein preparation (AqMf). ***To
investigate the mechanism
of M. fermentans antiapoptotic effect, the reduction of
mitochondrial transmembrane
potential (delta psi m) was measured. M. fermentans total proteins
LPMf and
MALP-2,
but not AqMf, inhibited the reduction of delta psi m. In addition,
M. fermentans
total proteins LPMf and MALP-2, but not AqMf, downregulated the
formation of
active
caspase-8.*** NF-kappaB was transactivated in cells treated with
M. fermentans
lipoproteins, and was essential for host cell survival, but not
for the inhibition
of TNFalpha-induced apoptosis by LPMf. *** Our results suggest
that the inhibitory
effect exerted by M. fermentans on TNFalpha-induced apoptosis in
U937 cells
is due
to the membrane lipoproteins of these bacteria.***
==================
More from FUNGAL VACCINES:
A) http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10792376&dopt=Abstract
The 19-kD antigen and protective immunity in a murine model of
tuberculosis.
Yeremeev VV, Lyadova IV, Nikonenko BV, Apt AS, Abou-Zeid C, Inwald J,
Young DB.
"The 19-kD antigen is a cell wall-associated lipoprotein present
in Mycobacterium
tuberculosis and in bacille Calmette-Guérin (BCG) vaccine strains.
Expression of
the 19-kD antigen as a recombinant protein in two saprophytic
mycobacteria-M. vaccae
and M. smegmatis-resulted in abrogation of their ability to confer
protection against
M. tuberculosis in a murine challenge model, and in their ability to
prime a DTH
response to cross-reactive mycobacterial antigens. Induction of an
immune response
to the 19-kD antigen by an alternative approach of DNA vaccination had
no effect
on subsequent M. tuberculosis challenge. These results are consistent
with a model
in which the presence of the 19-kD protein has a detrimental effect on
the efficacy
of vaccination with live mycobacteria. Targeted inactivation of genes
encoding selected
antigens represents a potential route towards development of improved
vaccine candidates."
B) http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11179309&dopt=Abstract
Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits
Mycobacterium smegmatis-induced
cytokine production by human macrophages in vitro.
Post FA, Manca C, Neyrolles O, Ryffel B, Young DB, Kaplan G.
Vaccination of mice with Mycobacterium vaccae or M. smegmatis
induces some protection
against M. tuberculosis challenge. The 19-kDa lipoprotein of M.
tuberculosis, expressed
in M. vaccae or M. smegmatis (M. smeg19kDa), abrogates this protective
immunity.
To investigate the mechanism of this suppression of immunity, human
monocyte-derived
macrophages (MDM) were infected with M. smeg19kDa. Infection resulted
in reduced
production of tumor necrosis factor alpha (TNF-alpha) (P < 0.01),
interleukin-12
(IL-12) (P < 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared
to
infection with M. smegmatis vector (M. smegV). Infection with M.
smeg19kDa and with
M. smegV had no differential effect on expression of costimulatory
molecules on
MDM, nor did it affect the proliferation of presensitized T cells
cocultured with
infected MDM. When MDM were infected with M. smegmatis expressing
mutated forms
of the 19-kDa lipoprotein, including non-O-glycosylated (M.
smeg19NOG), nonsecreted
(M. smeg19NS), and nonacylated (M. smeg19NA) variants, the reduced
production of
TNF-alpha or IL-12 was not observed. When the purified 19-kDa
lipoprotein was added
directly to cultures of infected monocytes, there was little effect on
either induction
of cytokine production or its inhibition. Thus, the immunosuppressive
effect is
dependent on glycosylated and acylated 19-kDa lipoprotein present in
the phagosome
containing the mycobacterium. These results suggest that the
diminished protection
against challenge with M. tuberculosis seen in mice vaccinated with M.
smegmatis
expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha
and IL-12 production,
possibly leading to reduced induction of T-cell activation."
C) http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12761093
Infect Immun. 2003 Jun;71(6):3146-54. Related Articles, Links
The Mycobacterium tuberculosis recombinant 27-kilodalton
lipoprotein induces
a strong Th1-type immune response deleterious to protection.
Hovav AH, Mullerad J, Davidovitch L, Fishman Y, Bigi F, Cataldi A,
Bercovier
H.
Department of Clinical Microbiology, Faculty of Medicine, The
Hebrew University,
Jerusalem, Israel.
Th1 immune response is essential in the protection against
mycobacterial intracellular
pathogens. Lipoproteins trigger both humoral and cellular immune
responses and may
be candidate protective antigens. We studied in BALB/c mice the
immunogenicity and
the protection offered by the recombinant 27-kDa Mycobacterium
tuberculosis lipoprotein
and the corresponding DNA vaccine. Immunization with the 27-kDa
antigen resulted
in high titers of immunoglobulin G1 (IgG1) and IgG2a with a typical
Th1 profile
and a strong delayed hypersensitivity response. A strong proliferation
response
was observed in splenocytes, and significant nitric oxide production
and gamma interferon
secretion but not interleukin 10 secretion were measured. Based on
these criteria,
the 27-kDa antigen induced a typical Th1-type immune response thought
to be necessary
for protection. Surprisingly, in 27-kDa-vaccinated mice (protein or
DNA vaccines)
challenged by M. tuberculosis H37Rv or BCG strains, there was a
significant increase
in the numbers of CFU in the spleen compared to that for control
groups. Furthermore,
the protection provided by BCG or other mycobacterial antigens was
completely abolished
once the 27-kDa antigen was added to the vaccine preparations. This
study indicates
that the 27-kDa antigen has an adverse effect on the protection
afforded by recognized
vaccines. We are currently studying how the 27-kDa antigen modulates
the mouse immune
response.
=====================
The first record that we can find on the OspA kind of antigen:
1983: Synthesis of the mitogenic S-[2,3-bis(palmitoyloxy)propyl]-N-
palmitoylpentapeptide
from Escherichia coli lipoprotein.
http://www.ncbi.nlm.nih.gov/pubmed/6347861?ordinalpos=131&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Several reports which make it appear as if the Pam3Cys type of antigen
was used
as an HIV vaccine adjuvant or is actually part of the HIV gp120 and
gp41 (I cannot
find out officially):
1) http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1421990&blobtype=pdf
2) http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=1349173
3) http://www.ncbi.nlm.nih.gov/pubmed/18524817?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
We found decreased Toll-like receptor 1 (TLR1) and TLR4 surface
expression in
HIV-infected U1 monocytic cells compared to the uninfected parental
U937 cell line
and decreased TLR message in alveolar macrophages (AMs) from HIV-
positive subjects.
In addition, stimulation with TLR1/2 ligand (Pam(3)Cys) or TLR4 ligand
(lipopolysaccharide)
resulted in decreased intracellular phosphorylated extracellular
signal-regulated
kinase and subsequent decreased transcription and expression of TNF-
alpha in U1
cells compared to U937 cells.
4) http://journal.kcsnet.or.kr/main/j_search/j_download.htm?code=B961118
(Korean
Journal where they blew up this HIV-Pam3Cys thing to look for
“We are currently using several mass spectral techniques to
characterize the
amino acid sequences of the Pam3Cys peptides found in the envelop
glycoproteins
of the HIV-1 and the Simian Immunodeficiency Virus (SIV).(17)
Convential FAB-MS
analysis using standard matrices, such as glycerol and nitrobenzyl
alcohol, is not
particularly effective for these molecules, largely due to their
tendency to aggregate”
[“their tendency to aggregate” …like what happened with LYMErix and
the Western
blot smudging, we think. We think they could never guarantee
completely free OspA
antigens in a vial of vaccine, and previous reports about HPLC assay
of OspA, I
suspect had a –prefiltering and pre-HPLC step because we always knew
OspA was a
sticky lipid and even sticks to itself, since Alan Barbour reported
that phenomenon.]
=====================
http://www.ncbi.nlm.nih.gov/pubmed/18162176?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Biochem Biophys Res Commun. 2008 Feb 29;367(1):41-6. Epub 2007 Dec
26. Links
The Ixodes scapularis salivary protein, salp15, prevents the
association of HIV-1
gp120 and CD4.
Juncadella IJ, Garg R, Bates TC, Olivera ER, Anguita J.
Department of Veterinary and Animal Sciences, University of
Massachusetts Amherst,
103 Paige Laboratory, 161 Holdsworth Way, Amherst, MA 01003, USA.
Ixodes scapularis salivary protein, Salp15, inhibits CD4(+) T cell
activation by
binding to the most-extracellular domains of the CD4 molecule,
potentially overlapping
with the gp120-binding region. We now show that Salp15 inhibits the
interaction
of gp120 and CD4. Furthermore, Salp15 prevents syncytia formation
between HL2/3
(a stable HeLa cell line expressing the envelope protein) and CD4-
expressing cells.
Salp15 prevented gp120-CD4 interaction at least partially through its
direct interaction
with the envelope glycoprotein. A phage display library screen
provided the interacting
residues in the C1 domain of gp120. These results provide a potential
basis to define
exposed gp120 epitopes for the generation of neutralizing vaccines.
https://www.aidsreagent.org/program_info.cfm#5
=======================
ON MEDLINE, searching for Pam3Cys and HIV or tripalmitoyl and HIV:
: J Virol Methods. 1988 Dec;22(2-3):173-82.Links
Distinction between HIV-1 and HIV-2 infection using novel synthetic
lipopeptide
conjugates as antigens in enzyme immunoassays.
Böltz T, Hummel RP, Tröger W, Rübsamen-Waigmann H, Biesert L, Müller-
Lantzsch N,
Koch P, Bessler W, Jung G.
Institut für Immunobiologie, Universität Freiburg, F.R.G.
A novel immunoassay technique using synthetic lipopeptide (Pam3Cys-
Ser) linked to
immunodominant peptide domains of HIV-1 and HIV-2 envelope proteins as
an antigen
adsorbent has been developed. Attachment of peptides to microtiter
plates can be
considerably improved with this method by employing the hydrophobic
properties of
lipopeptide. From the sera of 121 HIV-1 infected patients 117 reacted
with Pam3Cys-Ser-[HIV-1(598-609)cyclic
disulfide]. Five of 5 HIV-2 positive sera were positive with Pam3Cys-
Ser-[HIV-2(593-603)cyclic
disulfide]. Control sera failed to react with these conjugate
==================
Now, none of this will be in Pam Weintraub's book because I had
not published it all in one place before, except for the first page
I put up on what was wrong with LYMErix in 2003, and of course I
mentioned it to the FDA Vaccine Committee in 2001:
http://www.actionlyme.org/DICKSON_FDA_TEXT.htm
"OUTLOOK
"By what mechanism vaccination of the asymptomatic Bb infected
patients
is causing the Lyme like illness, we do not know exactly.
"Previous infection could be "priming" the immune system, as Denise
Huber
of Tufts has suggested, in "Identification of LFA-1 as a Candidate
Autoantigen in Treatment-Resistent Lyme Arthritis" July 31, 1998,
Science, Vol 281, p 703.
"or the vaccine is activating a dormant infection by the immune
dysregulation it causes, as demonstrated by the effect of Bb
infection and Osp A alone, on NK cells population, T cells,
neutrophils, and the effects on the various inflammatory
regulating biomoleclues, such as IL-10.
====================================================
The point and the fact is that the crooks were told about this in
1992 at the Cold Spring Harbor conference by Paul Duray in 1992
and probably earlier than that, in the 1989 IDSA Reviews:
http://www.actionlyme.org/Duray.htm
http://www.actionlyme.org/COLDSPRINGHARBOR.htm
and they all knew about it, since Dattwyler, Steere
Klempner and Wormser all reported about it from 1994
onward:
http://www.actionlyme.org/andersonpenisbiter.htm
(Everyone will have to read the DCF penis-biter report in order
to find the links)
THE CROOKS ALL KNEW THAT PEOPLE WHO HAD LOW ANTIBODY
CONCENTRATION WERE THE SICKEST, AND THEY ALL REPORTED THAT.
Lyme is not an inflammatory disease:
http://www.actionlyme.org/CRYMEDISEASE_CHP3_B.htm
This is a crime. The biggest one after 9/11:
http://www.actionlyme.org/070426.htm
Are we going to charge it as crime? or are we going to
hear about how Lyme causes sex, I mean sex causes Lyme
I mean providing orgasms for other people cures alcoholism,
or solar flares are cured by Simon Wessely's Questionaires
or eye of newt and wing of bat or we wimmins put a hex on
thems African sea birds so they'd fly to Long Guy-Land instead
of Miami on thems hurricanes or however Yale's psychiatric
whoring or blame-the-penis-ports (us'n wimmins) stories go...
Whoever figures out either Yale or psychiatry, wins.
Kathleen M. Dickson
http://www.actionlyme.org
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