Steere in Russia and Germany (and the Multiple Sclerosis form of Lyme)
Mort Zuckerman
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Subject: Steere in Russia and Germany (and the Multiple Sclerosis form
of Lyme)
Date: Jan 18, 2009 5:08 AM
=============================================
If Allen Steere was in charge of AIDS, it still would not be a
recognized disease. Steere went to Germany as well as Russia to
"instruct" the researchers there as to what they were to perceive as
regards testing for Lyme. He screwed-up-and-lied to Russia and he
screwed-up-and-lied to Germany. If Lyme is not an accidental release
from Plum Island there would have been no need for the Lie-Trips to
Europe.
http://www.actionlyme.org/index.htm
CHAPTER 22, THE Corrupticut Unions, The Dems, and James Amann
Connecticut, everyone will learn, is an extraordinary place. It's a
locale where the viciousness of WWII and Cold War clandestine warfare
is nearly 100% common; everyday life and everyday thinking. The
citizens of this state have the world's worst case of Keeping Up With
the Joneses. If a case study were the goal, anthropologists would
find that it is a literal fact that "a human rights activist is
insane," according to the vast majority of Connecticut residents.
Although bartering and finagling and skimming and cheating, and the
drugs, alcohol, hatred and paranoia are of course frowned-upon
publicly, no anthropologists point out that these happen to be The
Great White Way, in contrast to the sorts of social faux-pas that
Blacks are customarily accused. What we have here is the likes of a
Jew calling a German a Jew for his behavior. The Great Whites are
only great in their hypocrisy.
So bizarre is this state, that I had to listen to a lecture by a staff
member of State Representative James Amann's (D- Milford) whose name
also happens to be Kathleen. Amann's Kathleen tells me she is a
chemist and that she knows all about the testing for "Lyme Disease."
That surprises me because she would not be a chemist working for James
Amann if that were true. Amann's Kathleen tells me she knows more
about Lyme disease than I do because her mother had it and that her
mother got better from it. Usually people are criticized when making
general exclamations about medical conditions on the basis of a
relative's brief experience with it. In fact, the likes of Amann's
"chemist" are the very scary tards the Lyme criminals warn us about.
Amann's full time job is to be a fund-raiser for the Multiple
Sclerosis Society of America. He gets a percent of the money he
raises. Thus, he is so good at selling himself and his retarded
bullshit, he not only became a politician, he became the Connecticut
State Speaker of the House. The unions elect the democrats because
republicans have generally, in the past, been against big government
and unionized screw-driver-turners. The republicans in Connecticut
keep a low profile except for when they want to create the emergencies
of "bad parents and criminals" in order to defraud Uncle Sam over how
much "bad" goes on in this state, in order to not raise CT State
income taxes. It's a simple formulary where anyone who is not rich or
a State employee union member is fodder for this human hamburger
processor. The mere people have the same function they did in Machu
Picchu. The mere people are the materiél and maintenance of
slaughter needed to keep the political gods and the union gods happy
so it will rain dollars from China.
The National Institute of Neurological Disorder and Stroke's MS Chief,
Roland Martin, having been unable to prove that the Multiple Sclerosis
version of Lyme Disease/Relapsing Fever (undetectable with the current
Dearborn CDC diagnostic method) is due to autoimmune T cells returned
to his home country, Germany. One can go to the CRISP database and
enter Martin, Roland and search for all his grants.
http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen
Grant Number PI Name Project Title
1Z01NS002204-28 MARTIN, ROLAND Immunologic Mechanisms In
Experimental Autoimmune Diseas
1Z01NS002204-29 MARTIN, ROLAND Immunologic Mechanisms In
Experimental Autoimmune Diseas
1Z01NS002205-23 MARTIN, ROLAND INTERACTIONS BETWEEN THE HUMAN IMMUNE
SYSTEM AND ANTIGENS IN THE NERVOUS SYSTEM
1Z01NS002205-24 MARTIN, ROLAND INTERACTIONS BETWEEN THE HUMAN IMMUNE
SYSTEM AND ANTIGENS IN THE NERVOUS SYSTEM
1Z01NS002205-25 MARTIN, ROLAND INTERACTIONS BETWEEN THE HUMAN IMMUNE
SYSTEM AND ANTIGENS IN THE NERVOUS SYSTEM
1Z01NS002205-26 MARTIN, ROLAND Interactions Between The Human Immune
System And Antigen
1Z01NS002205-27 MARTIN, ROLAND Interactions Between The Human Immune
System And Antigen
1Z01NS002205-28 MARTIN, ROLAND Interactions Between The Human Immune
System And Antigen
1Z01NS002205-29 MARTIN, ROLAND Interactions Between The Human Immune
System And Antigen
Grant Number: 1Z01NS002205-29
Project Title: Interactions Between The Human Immune System And
Antigen
PI Information: Name Email Title
MARTIN, ROLAND
Abstract: This project examines the immunological mechanisms which
involved in the pathogenesis of autoimmune- and infectious diseases of
the central nervous system such as multiple sclerosis (MS) and chronic
Lyme disease. We characterize the fine specificity, function and
phenotype of T lymphocytes in the above diseases. These experiments
allow a better understanding of the foreign antigens that may trigger
autoimmune responses in MS and also of their function with respect to
cytokine secretion and chemokine receptor expression. Based on this
knowledge the project attempts to develop both specific
immunomodulatory treatments such as altered peptide ligands (APL) or
therapies that influence immune recognition in MS in a broader way.
Examples of the latter are the humanized antibody against the
interleukin-2 receptor alpha chain (Zenapax) or the phosphodiesterase
type IV inhibitor Rolipram. The trial with the APL peptide has been
concluded, and the data published. The clinical trials with Zenapax
and Rolipram are both supported through bench-to-bedside proposals.
Treatment of relapsing-remitting MS patients failing interferon-beta
with Zenapax has been well tolerated and successful, i.e. the primary
outcome has been met. Clinicial testing of Rolipram has been stopped
due to lack of efficacy and necessary changes of trial design.
Mechanistic studies along the experimental trials are ongoing and have
e.g. delineated that Zenapax acts primarily via expansion of
immunoregulatory NK cells. These studies will help us to understand
better the complex mechanism of action of these compounds and
eventually also the disease pathogenesis itself. All the clinical
projects are being pursued in close collaboration with the
Neurological Disease Section Section/Office of the Chief under Henry
F. McFarland, M.D. Another important project, which is currently being
pursued at NIB, NINDS, NIH, addresses the question which foreign
antigens, e.g. viruses or bacteria, may trigger the initiation or
exacerbations of disease via a mechanism referred to as molecular
mimicry. This concept refers to cross-recognition between
autoantigens, e.g. derived from the myelin sheath, and antigens
derived from foreign agents. For this purpose, we currently employ a
novel methodology called combinatorial peptide libraries in the
positional scanning format (ps-SCL) together with bioinformatic
approaches to identify the entire spectrum of stimulatory ligands for
autoreactive T cell clones derived from MS patients. In brief, we test
T cell clones with ps-SCL, which represent highly complex mixtures of
trillions of peptides, and deduce stimulatory peptide sequences from
these assays before we screen the databases of all known protein
sequences for potential stimulatory peptides. We are currently in the
process of developing this methodology further and anticipate that the
combination of ps-SCL and biometric data analysis will lead to
advances in the identification of target antigens for autoimmune
diseases, but also for tumor-specific lymphocytes or T cells that are
involved in infectious disease. ***As an example for the latter, our
data for organ-infiltrating T cells in chronic nervous system Lyme
disease*** already suggest that the immune response ***in the chronic
stage of the disease*** is directed against tissue autoantigens and
that this process is thus very similar to an autoimmune disease.
Currently, we also develop molecular biology strategies, i.e. the
expression of cDNA clones from MS brain in a special eukaryotic
expression system, for the identification of novel proteins that are
expressed in MS brains and serve as targets for the autoimmune
response. New projects include: The migration and differentiation of
neural stem cells into glial/neural cells. Integration of
immunological studies, MRI, clinical examination, expression profiling
and proteomics for the stratification of MS subtypes.
Public Health Relevance:
This Public Health Relevance is not available [because to admit that
Lyme causes MS is not politically correct].
Thesaurus Terms:
Lyme disease, autoantigen, human therapy evaluation, immunopathology,
monoclonal antibody, multiple sclerosis, nervous system disorder
chemotherapy, neuroimmunomodulation, phosphodiesterase inhibitor T
cell receptor, T lymphocyte, bacterial protein, chemokine receptor,
clinical trial, cytokine receptor, method development, natural killer
cell, nerve stem cell, pathologic process, receptor expression, virus
protein combinatorial chemistry, human subject, magnetic resonance
imaging, patient oriented research, peptide library
Institution:
Fiscal Year: 2004
Department:
Project Start:
Project End:
ICD: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
IRG: NIB
Now, let's take another look at what we know from the Steere/Dearborn
method to diagnose Lyme. The data, the files, the journal report
(Dressler/Steere) is in the public domain because it was entered as
evidence to the FDA's LYMErix vaccine meeting January 31, 2001, by
myself and not James Amann's chemist. The differences in the Western
Blotting between Steere's HLA and Roland Martin and Mark Klempner's
HLAs look like this:
Recall from Chp 3 that I got this data from Germany:
http://alpha1.mpk.med.uni-muenchen.de/bak/nrz-borrelia/miq-lyme/Frame-MiQ-microbiological53.html
From the Dressler/Steere report, when reported the result of his field
test ("Prospective study") of his proposed method:
Steere here redefines Lyme according to his own criteria because he
intended all along to state that Lyme was only a hypersensitivity
reaction in a knee. This, Dressler/Steere in Germany with the bogus
high passage strains and making up validation criteria like "receiver
operating characteristic," is research fraud or a medical hoax. This
is a "bogus article" as explained previously in Chapter 3.
The people who have Neuroborreliosis AND the inflammatory kind of Lyme
are rare even today. We only know a handful of such people who have
had neurologic Lyme for years in addition to the arthritis signs.
Steere found either 17 or 35 out of 237 patients who all thought they
had Lyme as diagnosed by other labs to also have Steere's idea of
Lyme. (Remember, Steere and Imugen were at that time using high
passage G39/40 and FRG in their Imugen Lab, when both strains are
illegal. One because it is German and the other because it as high
passage.)
If you read and re-read carefully, the full text of this Dressler
report, the Antigens in Europe report, and Steere's original standard
("look for changing and expanding IgM by sequential Western Blot"),
you will see that they wanted to contain (keep small) the number of
cases of Lyme Disease because they originally thought Lyme originated
in the United States in the Plum Island area.
Steere went to Germany as well as Russia to "instruct" the researchers
there as to what they were to perceive as regards testing for Lyme.
He screwed-up-and-lied to Russia and he screwed-up-and-lied to
Germany. If Lyme is not an accidental release from Plum Island there
would have been no need for the Lie-Trips to Europe.
It was all spin and scientific garbage.
You can see with your own eyeballs that Steere's kind of Lyme is a
hypersensitivity response.
"Receiver operating characteristic" means "the more antibodies, the
better," when, well, we would hope Steere would never be put in charge
of detecting plutonium for UNSCOM.
If Allen Steere was in charge of AIDS, it still would not be a
recognized disease.
A real student of this will look very, very closely at what Allen
Steere did and what Gary Wormser and his gang are trying to do at the
present time. It is a do-over of the first crime. They insist Lyme
is only a bad knee, when we know it is a very serious relapsing fever
type of spirochete because it is not in the blood most of the time
like the other relapsing fevers- which can be detected readily by
blood smear during the relapse.
Roland Martin in latest report (2006) basically reported the same
finding as his first (1988) report which had the result of Martin
coming to the United States:
* Martin R on autoimmune T cells in the CSF of Borreliosis victims
(full text scanned in)
Infection and Immunity, January 2007, p. 243-251, Vol. 75, No. 1
0019-9567/07/$08.00+0 doi:10.1128/IAI.01110-06
Copyright © 2007, American Society for Microbiology. All Rights
Reserved.
Cerebrospinal Fluid-Infiltrating CD4+ T Cells Recognize Borrelia
burgdorferi Lysine-Enriched Protein Domains and Central Nervous System
Autoantigens in Early Lyme Encephalitis{triangledown}
Jan D. Lünemann,1,5 Harald Gelderblom,1,6 Mireia Sospedra,1,2
Jacqueline A. Quandt,1 Clemencia Pinilla,3 Adriana Marques,4 and
Roland Martin1,2*
Neuroimmunology Branch, Cellular Immunology Section, National
Institute of Neurological Disorders and Stroke, National Institutes of
Health, Bethesda, Maryland 20892,1 Institute for Neuroimmunology and
Clinical MS Research (INiMS), Center for Molecular Neurobiology
Hamburg (ZMNH), University Clinic Eppendorf, Falkenried 94, 20251
Hamburg, Germany,2 Mixture Science and Torrey Pines Institute for
Molecular Studies, San Diego, California 92121,3 Laboratory of
Clinical Infectious Diseases, National Institute of Allergy and
Infectious Diseases, National Institutes of Health, Bethesda, Maryland
20892,4 Laboratory of Viral Immunobiology, The Rockefeller University,
New York, New York 10021,5 Department of Neurology and Psychiatry,
Charité Medical Center, Humboldt University, 10098 Berlin, Germany6
Received 14 July 2006/ Returned for modification 15 September 2006/
Accepted 10 October 2006
Neurological manifestations of Lyme disease are usually accompanied by
inflammatory changes in the cerebrospinal fluid (CSF) and the
recruitment of activated T cells into the CSF compartment. In order to
characterize the phenotype and identify target antigens of CSF-
infiltrating T cells in early neuroborreliosis with central nervous
system (CNS) involvement, we combined T-cell cloning, functional
testing of T-cell responses with positional scanning synthetic
combinatorial peptide libraries, and biometric data analysis. We
demonstrate that CD4+ gamma interferon-producing T cells specifically
responding to Borrelia burgdorferi lysate were present in the CSF of a
patient with acute Lyme encephalitis. Some T-cell clones recognized
previously uncharacterized B. burgdorferi epitopes which show a
specific enrichment for lysine, such as the heat shock-induced
chaperone HSP90. Degenerate T-cell recognition that included T-cell
responses to borrelia-specific and CNS-specific autoantigens derived
from the myelin protein 2',3'-cyclic nucleotide 3'-phosphodiesterase
(CNPase) could be demonstrated for one representative clone. Our
results show that spirochetal antigen-specific and Th1-polarized CD4+
lymphocytes infiltrate the CSF during monophasic CNS symptoms of Lyme
disease and demonstrate that cross-recognition of CNS antigens by B.
burgdorferi-specific T cells is not restricted to chronic and
treatment-resistant manifestations.
We say, okay. What do we know from the MS-Lyme experiment?
Basically that Lyme can be mistaken for Multiple Sclerosis since there
is really no way to tell them apart based on the clinical and the lab
data, combined. There is no diagnostic class of badly cloned T cells,
such that you could run a comparative T-cell check on an MS person or
a Lyme person. Everyone does their own personal T cell (and B)
warping based on their particular antigen-varying spirochetes and
their genetic background. Remember from the RICO patents chapter, CDC
officer Alan Barbour said that Lyme infected people could have just
overwhelmed immune systems from this non-clonality, the variety of
original spirochetes, and the infinite variations in the blebs.
Our immune systems have gone haywire.
And everyone is different.
And if you ask a Lyme specialist, they will tell you too: Everyone is
different with their daily and hourly and typical Lyme complaints. It
really is relentless torture. One minute you're almost fine and you
can get the laundry done (since this chore only takes 30 seconds at
time), and the next minute you have a splitting migraine on one side
of your head. Then later in the day you'll have sharp pains here and
there and you're dead tired. The headache is literally blinding in
that your eyes won't focus or even work together (one goes one way and
the other goes another), and all you can think about is SHUT OFF THE
LIGHTS AND THE NOISE!! and LET ME CRAWL INTO A CAVE and EVERYONE SHUT
UP!!!
'Just like the flu. Every little noise bothers you and you would kill
for sleep, since that's the only escape from it.
Sunlight is like metal cylinders stabbing into your eye sockets and
your thoughts turn to ghosts, since that's what you've become. You
hide from the sunlight. You walk around the windows because you can't
bear to get any near your head. It is something no one can understand
unless they've tried it or have very recently had a very bad flu.
You're saying to yourself (foolishlessly; as a result of your previous
American establishment brainwarping) "Maybe I should call a doctor?!!"
Then you remember.
There is no one to call.
Maybe by 5 o'clock PM you feel almost normal (for everyday Lyme) again
but by 7 you're ready to collapse.... That's Lyme Disease- an all day
long all year long all life long variety show that would make Job look
like the Princess and her Pea.
As we Lymies always say, If you don't believe us, by all means, try
it.
Bill Chinook (Bruce Springsteen's E- Street Band, living in Maine)
killed himself last summer (2007) and it wasn't because he was looking
for sex or attention. He did it because he could not stand the misery
of this disease any more. Say what you will, but take the risk of
eternal damnation for not being sympathetic, since "CARE" is what the
"is" is about life itself. You have already seen enough evidence that
this disease causes nearly limitless misery.
You can see with your own eyeballs that the testing for it is a
criminal matter and that the persistence past treatment matter was
already a known and a given in 1975- says the representative of US
Military Medical in Bethesda.
MS Laboratory positive in Lyme: Oligoclonal bands in the CSF and T-
weighted images (ischemia or mini-strokes) on brain MRI:
Martin R on oligoclonal bands in the CSF (formerly a marker of
Multiple Sclerosis) of Borreliosis victims
See also the BIOMARKERS, BRAIN PERMANENT, and the FUNGAL VACCINES
chapters because this MS data, the OspA-induced-immune-suppression-and-
activation-of-viral-infections outcomes, the strange common failure
method of other fungal vaccines (Tuberculosis and Lyme), and the
mycoplasma-and-fatigue and mycoplasma-and-cancer data, all appear to
be related to the chronicity. In other words, if not for the
"Barbour's Stealth Bombers" or the Barbour "Bacterial Star Wars" or
what I simply call the flak aspect of the chronic shedding of surface
antigens- something relapsing fever spirochetes do anyway - in
combination with the OspA types of shed antigen, seem to be the key
combo to produce a wicked bioweapon.
1) Chronic lies about what's a positive test
2) Denial of the potential diagnostic value of anti-flagellar
antibodies
3) CDC's lies even to CT AG Richard Blumenthal
4) Stealth, microscopic tick
5) Deployment of very abusive tactics against victims and their
treaters (McSweegan and Fish)
6) The Wreckage of OspA vaccination and the deliberate non-reporting
of systemic adverse events (LYMErix causes a Lyme-like illness because
chronic Lyme and LYMErix Disease® are the same thing: all the immune
suppression outcomes of chronic Lyme including the bad, bad,
irresponsible T cells in the spinal fluid and not only the knee...)
7) Deployment of the psychiatric morons, who still won't admit they're
being used by the Bigs and the "government" against the very sick Gulf
War I veterans (Humanity and the Periodicy of Social Delusions: Let's
see, the Jews and the Goyem, the Inquisition, Martin Luther, witch
hunts, the Divine Rights of Kings, Psychiatry, McCarthyism, The War on
Terror, Political-US-Attorneys, Polish-Iranian ICBM interceptors...)
8) The suppression of immune-suppression facts; the denial that this
is anything BUT an inflammatory disease
9) Ferocious attacks on mothers with children with Congenital Lyme.
The flat-out denial of Congenital Lyme
and the latest distortion of facts,
10) Lyme came from Europe.
Bologna. It's all relapsing fever and this OspA one just happened to
be OspA-in-a-hard-bodied-tick 10 miles from where they do such
experiments. It's nearest relatives are B. hermsii and B. anserina
(African bird spirochetes), based on differences in flagellar DNA
(Picken, 1992). The rest of the characteristic of all tick borne
spirochetes is that after the linear chromosome and the wave length
code, it's almost all a matter of the plasmid DNA.
Metabolically, we can discover few differences between them. If a
borrelia is going to take to a tick two factors must be present.
Enough mutants have to be present to generate the right surface
antigens to adhere to whatever they need inside a tick, and then more
of them acquire bacteriophage-vectored DNA from other organisms.
Since Lyme came from the Plum Island area and mycoplasma and E.coli
share the same general OspA, we guess that the OspA antigen was some
DNA shared by these organisms who happen to share the same phage.
Whether or not this was deliberate or an accident, no one with Lyme
really cares. Think about it. Once you are terribly sick from this
disease, all you can think about it how you can get better and the
utter absurdity of the denial by the Lyme crooks of the existence of
their very own reports describing how very sick we are.
Then as the years go by and you get 100% better but then relapse and
discover it's all been a hoax. Your blood boils and you try to reach
back into your genetic past for a fragment of endowment or a debt to
repay or famous solider or a saint in your lineage or the one with
your name or the saint of your day - any and all of the good people of
the past who you represent today - that gives you the "We Are" to tear
these evil IDSA/ALDF/Yale lying Lyme bastards apart and throw them
into the inferno.
That they would harm so many people and take pleasure in witnessing
the double torture of their victims?
Who would be such a coward as to not to fight them? To me, not to
fight these evil pitbulls of "medicine" once I found out what they did
is unimaginable. It would be like standing by and doing nothing while
some grizzly old crazy drunk kidnaps a baby out of a shopping cart and
beats it with a baseball bat. That's how I see the people who do
nothing to help us. We're sick and we're innocent. Tick bites are
not a character flaw.
Why am I writing this? Why am I telling this story?? Who in a
million years imagines this sort of thing will be dumped in their
laps? What kid wishes to be a corporate cop? What kid dreams about
one day punking the latter day NAZIs? Or that fate would land them on
nearly the same town on the southeastern Connecticut coast where there
was no support group for this strange-but-not-new disease that bears
the town's name, in 1993, 18 years after the disease was discovered by
the famous mother (and not father or MD), Mrs. Polly Murray.
NO SUPPORT GROUP IN THE COUNTY OF LYME in 1993 ???
What was I saying about Corrupticut?
===========ROLAND MARTIN'S FORMER WEBPAGE AT THE NIH ============
Cellular Immunology Section
Roland Martin, M.D., Investigator
Dr. Martin received his medical training at the University of
Würzburg, Germany, and prepared his M.D. dissertation with Jörg
Draeger at the University of Hamburg, Germany. Following a post-
doctoral fellowship with Hans-Wolfgang Kreth, Institute for Virology
and Immunobiology, Würzburg, and a neurology residency with Hans-Georg
Mertens, Department of Neurology, Würzburg, he received additional
post-doctoral training with Henry McFarland, Neuroimmunology Branch,
NINDS, studying cellular immunity in multiple sclerosis (MS). Dr.
Martin joined the faculty at the Department of Neurology, Tübingen,
Germany, with Johannes Dichgans, and conducted research in
neuroimmunology. Dr. Martin continued his research at the
Neuroimmunology Branch of the NIH and the Department of Neurology,
University of Maryland at Baltimore with Kenneth Johnson. In 1997 he
moved to the NINDS where he is the Acting Chief of the Cellular
Immunology Section, Neuroimmunology Branch. He has received the
Heinrich Pette Award of the German Neurological Association and a
Heisenberg Professorship of the Deutsche Forschungsgemeinschaft. Dr.
Martin's laboratory investigates the cellular immune system in
multiple sclerosis and chronic Lyme disease and, together with Henry
McFarland, develops novel treatment modalities for MS.
Staff (All foreigners; to continue with the PsyOps on Lyme??)
* Bibiana Bielekova, M.D., Staff Clinician biel...@ninds.nih.gov
* Gregg Blevins, M.D., Clinical Fellow blev...@ninds.nih.gov
* Erik Cabral, B.S., Student, (301) 496-0518
* Ricardo Cassiani-Ingoni, Ph.D., Postdoctoral Fellow
cass...@ninds.nih.gov
* Azita Kashani, B.S., Research Assistant, (301) 496-0518
* Dr. Paolo A. Muraro, M.D., Ph.D., Senior Research Fellow
mur...@ninds.nih.gov
* Elisabetta Prat, M.D. pr...@ninds.nih.gov
* Susan Scrivner, M.S., Research Assistant scri...@ninds.nih.gov
* Mireia Sospedra, Ph.D., Postdoctoral Fellow sosp...@ninds.nih.gov
* Xiang Wang, M.S., Senior Research Assistant, (301) 402-4488
wan...@ninds.nih.gov
Research Interests:
We are interested in a better understanding of how the cellular immune
system in multiple sclerosis (MS) patients reacts to autoantigens of
the central nervous system. Our research includes studies on the
molecular mechanisms of T cell recognition, i.e. how T lymphocytes
recognize antigens in the context of MS-associated HLA-DR antigens, in
particular HLA-DR15 Dw2. These experiments address the functional and
phenotypic repertoire of T cells responding to various myelin antigens
including myelin basic protein (MBP), 2’3’-cyclic nucleotide-3’
phosphodiesterase (CNPase), proteolipidprotein (PLP), myelin
oligodendroglia glycoprotein (MOG), and myelin oligodendroglia basic
protein (MOBP), but also which foreign agents may trigger autoreactive
T cells via molecular mimicry. Through collaborations, we develop
novel methods to study molecular mimicry. Along studies of the
immunologic pathomechanisms of MS, we try to design new
immunotherapeuties based on the concepts evolving from the above work.
It is our final goal to develop these new therapeutic strategies until
they are applicable in MS patients and test them in phase I/II trials.
Candidate therapies which are currently being studied are altered
peptide ligands based on MBP peptide (83-99) as a highly specific
immunomodulation, phosphodiesterase type IV inhibitors to block Th1-
cytokines, and the administration of a humanized monoclonal antibody
against the IL-2 receptor a-chain expressed on activated T cells. In
treatment trials as well as in longitudinal studies of disease
activity in MS patients immunologic disease markers (measured by
ELISA, quantitative PCR, cDNA microarrays, T cell frequencies and
specificity) are correlated with the clinical course and disease
activity as assessed by MRI. These experiments shall not only help us
to evaluate the efficacy of novel treatments, but also try to prove
the pathogenetic concepts derived from animal studies.
Selected Recent Publications:
*
Kondo, T., Cortese, I., Markovic-Plese, S., Wandinger, K.-
P., Carter, C., Brown, M., Leitman, S., Martin, R. (2001) Dendritic
cells signal T cells in the absence of exogenous antigen., Nat.
Immunol. 2, 932-938.
*
Kondo, T., Cortese, I., Markovic-Plese, S., Wandinger, K.-
P., Carter, C., Brown, M., Leitman, S., Martin, R. (2001) Dendritic
cells signal T cells in the absence of exogenous antigen., Nat.
Immunol. 2, 932-938.
*
Bielekova, B., Goodwin, B., Richert, N., Kondo, T., Eaton,
J., Afshar, G., Antel, J. Frank, J.A., McFarland, H.F., Martin, R.
(2000) Encephalitogenic potential of myelin basic protein peptide
(83-99) in multiple sclerosis – Results of a phase II clinical trial
with an altered peptide ligand. , Nature Medicine 6, 1167-1175.
*
Hemmer, B.*, Gran, B.*, Zhao, Y., Marques, A., Pinilla, C.,
Pascal, J., Tzou, A., Kondo, T., Cortese, I., Bielekova, B., Straus,
S., McFarland, H.F., Houghten, R., Simon, R., Martin, R. (1999)
Identification of candidate epitopes and molecular mimics in chronic
Lyme disease. , Nature Medicine 5, 1375-1382.
*
Hemmer, B., Fleckenstein, B, Vergelli, M., Jung, G.,
McFarland, H.F., Martin, R., Wiesmüller, K.-H. (1997) Identification
of high potency microbial and self ligands for a human autoreactive
class II restricted T cell clone., J. Exp. Med. 185, 1651-1659 .
All Selected Publications
Contact Information:
Dr. Roland Martin
Cellular Immunology Section
Neuroimmunology Branch, NINDS
Building 10, Room 5B16
10 Center Drive, MSC 1400
Bethesda, MD 20892-1400
Telephone: (301) 402-4488 (office), (301) 402-4488 (laboratory),
(301) 402-0373 (fax)
Email: mar...@ninds.nih.gov
Last updated Friday, September 13, 2002
Comments or questions? Send email to intraw...@ninds.nih.gov
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> CHAPTER 23, THE DISTRICT OF CORRUPTICUT USDOJ, PORNOGRAPHY, AND BANTAM
> LAKE
Steere went to Germany as well as Russia to "instruct" the
researchers
there as to what they were to perceive as regards testing for Lyme.
He screwed-up-and-lied to Russia and he screwed-up-and-lied to
Germany. If Lyme is not an accidental release from Plum Island there
would have been no need for the Lie-Trips to Europe.
YOU SAID IT K------IN REF TO STEERE GOING TO RUSSIA & GERMANY TO
"INSTRUCT""" THEIR RESEARCHERS ETC. WHAT A JOKE -----THE DISEASE WAS
KNOWN OVER THERE FOR OVER 100 YRS. AND THE JERK STEERE FIRST SAID IT
WAS FROM A VIRUS AND PRESCRIBING ASPIRIN.
IT WAS ACTUALLY POLLY MURRAY WHO DID MOST OF THE SLEUTH WORK......YOUR
RIGHT THAT'S ALL HE PUSHES NOW IS THE SWOLLEN KNEE DEAL----------THAT
BETINA WILSKE IS NOW ON HIS SIDE ALSO .......NO WONDER POLLY MURRAY
HAS NOTHING TO DO WITH THE CREEP STEERE. ......
ALSO AT DR. B'S HEARING IT WAS MENTIONED DESPITE IN EUROPE USING LONG
TERM ANTIBIOTICS ---DATTYLER SHOT OUT "THEY HAVE A DIFFERENT STRAIN IN
EUROPE"-----HMMMM ------NOTHING BUT A BUNCH OF DEVILS.
OLD ARTICLES BY STEERE STATING SERONEGATIVITY IS A REAL PHENONOMEN
PLUS LATE STAGE LYME HAS THE SYMPTOMS OF TERTIARY SYPHILIS.
GREAT SCIENTISTS ---THEN A COMPLETE ABOUT FACE ---MONEY - PAYOFFS-----
LIKE I TOLD A CERTAIN FEW OTHER MD'S "WE ALL HAVE TO DIE AND WE ALL
HAVE TO ANSWER TO THE LORD"
I SAW THAT LETTER ON YOUR SITE IN REF TO THE GROUP SAYING WE HAVE TO
GET RID OF THE LDF'S BOGUS JOURNAL ----THAT JOURNAL WAS EXCELLENT --
AND THE REMARK SAYING KAREN FORSCHNER IS CRAZY --AND WE HAVE TO GET
THOSE LYME PROTESTERS ETC.
I DON'T BLAME YOU FOR YOUR ANGER.......THEY WILL BE WHEN THEIR TIME
COMES DANCING ON THE HOT COALS.....IN THE FURNACE DOWN BELOW.
It was all spin and scientific garbage. SURE WAS - & HOW COULD SOME OF
THOSE EUROPEANERS FALL FOR THAT GARBAGE.............
You can see with your own eyeballs that Steere's kind of Lyme is a
hypersensitivity response.
"Receiver operating characteristic" means "the more antibodies, the
better," when, well, we would hope Steere would never be put in
charge
of detecting plutonium for UNSCOM.
If Allen Steere was in charge of AIDS, it still would not be a
recognized disease.
YES POST AIDS SYNDROME---------------------AN AUTOIMMUNE DISEASE-
STICK THEM WITH STERIODS AND METHOTREXATE.