Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."
 


18 May 2017


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PDFs
CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
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BarbourFishpdf.pdf
 

Pathogenic Fungi

Predicting all of GW Bush's warcrimes, Oct 2000

Trainer

 

 


 

141120-- This chapter will probably be re-written (originally written Nov, 2007) or included in another chapter when I reduce it all for the New "Khan Academy" of Lyme Cryme.  Much of the same data is included in other reports - see the homepage.  KMDickson


 


The German scientist Roland Martin, former head of the NINDS-Multiple Sclerosis Division because he found Lyme to be a cause of MS, quit his job at the NIH went back home to Germany once he found that the TLR2 agonist OspA was actually the cause of the MS presentation of Lyme. 

Meanwhile, in his lab at the NIH were all foreign students (see the bottom of this page) because... they wanted the DISINFORMATION of "auto-immune T cells as the cause of MS" to spread out around the world, once these students when home to their native countries.

Martin quit when he found out he had been used and that, in fact, the LYMErix vaccine, OspA, was immunosuppressive (caused seronegative disease) and was responsible for the chronic illness:

Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.

Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 [manages flagellin] in human monocytes.


CHAPTER 18;  Corrupticut Unions and Politicians
* Martin R on autoimmune T cells in the CSF of Borreliosis victims (full text scanned in)
 

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.

Half the people with Neuroborreliosis have detectable "proteins" or invasion with inflammatory lymphocytes, according to Andrew Pachner in 1989.  Cerebrospinal fluid analysis (looking for cells), and EMG
are not "clinical" criteria.  In 1989 it was known by IDSA that Lyme meningitis was mistakenly missed because it is an ASEPTIC meningitis (low or no cells in the CSF): IDSA_GREATIMITATOR.htm

Steere in 1991, when he published about seronegative Lyme using the Dattwyler/Volkman seronegative Lyme T-cell proliferation assay, reported that 4/9 of his Borrelia lab workers had been exposed to Borrelia (we assume this was due to inhalation of spheroplasts, as discussed by the US Army manual on infectious diseases in Haiti).

Steere reported here in Dressler/Steere that either 17 or 35 out of 237 patients who all thought they had Lyme as diagnosed by other labs to had 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.  It's tough to tell exactly what he did, as Steere's reports tend to be intentionally illogically garbled and impossible to follow. 

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 ============

 


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:



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: martinr@ninds.nih.gov


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CHAPTER 23, THE DISTRICT OF CORRUPTICUT USDOJ, PORNOGRAPHY, AND BANTAM LAKE