LymeNet Home LymeNet Home Page LymeNet Flash Discussion LymeNet Support Group Database LymeNet Literature Library LymeNet Legal Resources LymeNet Medical & Scientific Abstract Database LymeNet Newsletter Home Page LymeNet Recommended Books LymeNet Tick Pictures Search The LymeNet Site LymeNet Links LymeNet Frequently Asked Questions About The Lyme Disease Network LymeNet Menu

LymeNet on Facebook

LymeNet on Twitter




The Lyme Disease Network receives a commission from Amazon.com for each purchase originating from this site.

When purchasing from Amazon.com, please
click here first.

Thank you.

LymeNet Flash Discussion
Dedicated to the Bachmann Family

LymeNet needs your help:
LymeNet 2020 fund drive


The Lyme Disease Network is a non-profit organization funded by individual donations.

LymeNet Flash Post New Topic  New Poll  Post A Reply
my profile | directory login | register | search | faq | forum home

  next oldest topic   next newest topic
» LymeNet Flash » Questions and Discussion » Medical Questions » 2008 ILADS Searching for autoimmunity in "antibiotic-refractory" Lyme arthritis.

 - UBBFriend: Email this page to someone!    
Author Topic: 2008 ILADS Searching for autoimmunity in "antibiotic-refractory" Lyme arthritis.
TerryK
Frequent Contributor (5K+ posts)
Member # 8552

Icon 1 posted      Profile for TerryK     Send New Private Message       Edit/Delete Post   Reply With Quote 
1: Mol Immunol. 2008 Jun;45(11):3023-4. Epub 2008 Apr 18. Links

Searching for autoimmunity in "antibiotic-refractory" Lyme arthritis.Stricker RB, Johnson L.

International Lyme and Associated Diseases Society, P.O. Box 341461, Bethesda, MD 20827-1461, United States.

In two recent articles published in Molecular Immunology, Steere and colleagues continue their search for an autoimmune mechanism of arthritis in patients who have failed short-course antibiotic therapy for Borrelia burgdorferi, the spirochetal agent of Lyme disease.

As in previous attempts, the authors fail to elucidate a molecular mimicry mechanism for the putative autoimmune process, leading to the conclusion that there is no credible scientific evidence for a post-infectious autoimmune mechanism of arthritis in chronic Lyme disease.

PMID: 18395260 [PubMed - in process]

Posts: 6285 | From Oregon | Registered: Jan 2006  |  IP: Logged | Report this post to a Moderator
luvs2ride
Frequent Contributor (1K+ posts)
Member # 8090

Icon 1 posted      Profile for luvs2ride     Send New Private Message       Edit/Delete Post   Reply With Quote 
[spinning smile] [Big Grin]

Well, I could have told them that. My first rheumatologist, when I was first diagnosed with rheumatoid arthritis and I showed him my positive lyme test, said "The Lyme is gone and now you are left with RA". I stared in shock and asked "How do you know the Lyme is gone?" No reply.

The rheumy refused to test me for mycoplasmas, strep, coinfections, H. Pylori, despite my medical history of all these infections and my request that he do so.

My new rheumy who follows ILADS ran all those tests. In fact, she runs tests routinely. She has been hauled before the medical review board once. She won her case and now she gives them bloodtests. Lots of bloodtests. I accuse her of trying to cure me by bloodletting and calling it bloodtests.

Fact is though, I consistently, I repeat...CONSISTENTLY...test positive for a number of infections. Babs WA-1(just got my first negative Babs after 1 yr of positives), Mycoplasmas, CPN, EBV, H. Pylori (gone now). I am sure I could sue my first rheumy for refusing to test me.Don't you think?

What a bunch of losers is the field of rheumatology. First thing he said to me "We don't know what causes it (RA) and we don't know how to cure it but we can slow it down." Then when I want to rule out some possible causes, he refuses. Who is he to thumb is nose at anything? He already admitted he doesn't know anything. How can he be sure everyone else is wrong?

And how can he or anyone else know lyme is gone? What definitive test do they have to be so sure?

Losers, losers, losers [Razz] Let them test til the cows come home. They will never find the answer they want.

--------------------
When the Power of Love overcomes the Love of Power, there will be Peace.

Posts: 3038 | From america | Registered: Oct 2005  |  IP: Logged | Report this post to a Moderator
smjkoj
Member
Member # 15241

Icon 1 posted      Profile for smjkoj     Send New Private Message       Edit/Delete Post   Reply With Quote 
Can someone translate this for me? My husband has severe joint pain which the LLMD has called "lyme arthritis".

Thanks!

Posts: 26 | From Virginia | Registered: Apr 2008  |  IP: Logged | Report this post to a Moderator
Lymetoo
Moderator
Member # 743

Icon 1 posted      Profile for Lymetoo     Send New Private Message       Edit/Delete Post   Reply With Quote 
quote:
Originally posted by smjkoj:
Can someone translate this for me? My husband has severe joint pain which the LLMD has called "lyme arthritis".

Thanks!

From what I gather.. they are saying they still can't prove that Lyme causes an autoimmune response. {which I agree is not there...it's INFECTION!}

--------------------
--Lymetutu--
Opinions, not medical advice!

Posts: 95974 | From Texas | Registered: Feb 2001  |  IP: Logged | Report this post to a Moderator
TerryK
Frequent Contributor (5K+ posts)
Member # 8552

Icon 1 posted      Profile for TerryK     Send New Private Message       Edit/Delete Post   Reply With Quote 
That's my understanding too. The IDSA denies chronic lyme disease even exists, they call it post lyme and consider it an autoimmune problem.

ILADS is saying there is no evidence that it is an autoimmune problem.

Terry

Posts: 6285 | From Oregon | Registered: Jan 2006  |  IP: Logged | Report this post to a Moderator
Shosty
Unregistered


Icon 1 posted            Edit/Delete Post   Reply With Quote 
Lyme triggered autoimmunity in both myself and my daughter. My daughter has a very high ANA, low complements and also positive anti-DNA. I have had high ANA, very high cardioCRP, and a skin biopsy positive for either lupus or dermatomyositis, both autoimmune. I get sick in the sun.

My daughter got type 1 diabetes, an autoimmune illness, when she was 4, through "molecular mimicry," after coxsackie, a virus. She is genetically predisposed for this, and most people who get coxsackie certainly don't go on insulin.

Many tests are cross-reactive for Lyme or symphilis and lupus etc. Symptoms are similar. Antibiotics are used by some doctors for any autoimmune illness, and disparaged by others.It is all very confusing.

These issues are very, very murky, and while the rheumatologists may seem rigid, the Lyme community can too. Things are so polarized that patients often suffer.

I was on antibiotics for 6 years, way too long. No more progress was being made with my Lyme-induced neuropathy or my autoimmune problems. It was difficult to get off the abx. But I made more progress eliminating food allergens for a few days, than I did with the last 4 years of antibiotics (some progress did occur in the first year or two). Everyone is different, but there are other approaches that we can all try.

Those of us with HLA-DR4 genetic types may very well have both an infection and an autoimmune reaction to the infection. This is what can happen with strep, again, with a small percentage of people who are genetically prone.

The rheumatolgists slam the Lyme community, and the Lyme community slams the rheumatologists, when we should all be mutually respectful and work together.

Patients suffer from oversimplification and polarization. Maybe we Lyme sufferers could begin the change.

IP: Logged | Report this post to a Moderator
AliG
Frequent Contributor (1K+ posts)
Member # 9734

Icon 1 posted      Profile for AliG     Send New Private Message       Edit/Delete Post   Reply With Quote 
Very Interesting!

So the recent findings of my Neuro-Ophth that I likely have "MS secondary to Lyme" possibly due to "molecular mimicry" was something of an "IN YOUR FACE" to Steere & colleagues.

Oh, I like my Neuro-Ophth VERY MUCH!!!! [Big Grin]

[woohoo]

[cussing] TAKE THAT YOU EVIL IDSANS!!!! [cussing]

[woohoo]


Maybe I SHOULD go for that LP. If only I knew for certain what it would show. I really can't afford to risk any false negatives in the hands of the insurance companies.

They could probably use one to try to negate all my positives on bloodwork and say that now it's ONLY MS and refuse to pay for Lyme Tx.

Then again if they did that, I COULD always go collect a bunch of ticks from my yard, bring them to the doctor & say I waited for bulls-eyes and didn't get any but I'm still feeling sick.

Maybe if I get the ticks tested I can find out any still undiscovered co-infections I might have.

Actually getting some ticks tested might not be such a bad idea. (I was only kidding about doing something so dishonest. I'm sure the Karma would bite me in the butt. [Roll Eyes] )

I have to go start another thread to see if I can find out how to get a tick-drag done.

Thanks for posting this!
[hi]
Ali

--------------------
Note: I'm NOT a medical professional. The information I share is from my own personal research and experience. Please do not construe anything I share as medical advice, which should only be obtained from a licensed medical practitioner.

Posts: 4881 | From Middlesex County, NJ | Registered: Jul 2006  |  IP: Logged | Report this post to a Moderator
Shosty
Unregistered


Icon 1 posted            Edit/Delete Post   Reply With Quote 
We regret doing the LP's. So many people with Lyme have negative LP's, and our negative results were, in fact, used against us, not by insurance, but by MD's to validate their position that we have autoimmune problems, and not Lyme. This was several years back when we most definitely had active Lyme.

It may sound strange, but in a way, my post above backs up what Steere et al say, but only part of it. In other words, I have come to believe that Lyme (and other bacteria, probably) trigger lupus or other autoimmune problems (maybe MS too) and that it is possible that these other disorders do in fact sometimes continue independent of Lyme, after the Lyme itself has been controlled (I won't say cured) with abx.

That said, I think it is a whole lot harder to tell when the Lyme has been addressed, than "they" do, and I believe, of course, that it takes a whole lot longer on abx to deal with Lyme, than Steere and friends say.

So, I agree with the possibility that some of us do really have some sort of post-Lyme autoimmune syndrome, which has a life of its own after abx treatment, possibly through molecular mimicry (who knows?).

At the same time, I think some of us have autoimmune problems/test results that will go away with Lyme treatment, that are caused by the bacteria/toxins.

And some of us have symptoms that resemble autoimmunity but it is really Lyme alone, and nothing to do with antibodies.

And, finally, it is even possible that some of us have autoimmune problems from other causes, and are blaming our symptoms on Lyme, when we don't have Lyme at all.

I think that about covers the possibilities!

The problem is that Steere et al want to oversimply things and say that everything is post-Lyme syndrome, and therefor abx should be limited.

But we Lyme sufferers (speaking of myself, in the past, at least) have also tried to simplify things, and therefore denied the very valid possibility that there are some consequences to Lyme that cannot be addressed with abx.

Even some really great LLMD's have written about the autoimmune aspects of Lyme for people with the HLA-DR4 genetic type, and that their Lyme is harder to treat. In fact, Jones is the first one to tell us about all this. From everything I have written, you can see that there are many ways to interpret this.

At any rate, after many years of all this, I think most of us end up coming at our illness with a multi-pronged approach, often using alternative methods, either with or instead of abx. I don't even care anymore whether I have Lyme or lupus. Isn't that strange?

p.s. my daughter has type 1 diabetes, which was triggered at age 4, by the coxsackie virus. She is now 18. She has had Lyme as well, and other problems. The concept of molecular mimicry is just part of our ordinary life around here, since type 1 diabetes permeates everything we do. It is real.

IP: Logged | Report this post to a Moderator
Parisa
LymeNet Contributor
Member # 10526

Icon 1 posted      Profile for Parisa     Send New Private Message       Edit/Delete Post   Reply With Quote 
Shosty,

You're the first poster here that I've seen with possible dermatomyositis induced by Lyme. My husband has lyme induced dermatomyositis. Dermatomyositis is uncommon (or used to be) that it's difficult to get a pool of people together. Even if you go to myositissupport.net, the numbers there are so small.

Sorry to hear you're sick but it is nice to find one more Lymie with dermatomyositis symptoms.

By the way, IVIG is helping my husband with muscle weakness/destruction and has taken away alot of the pain he was having (neuropathy).

Posts: 984 | From San Diego | Registered: Nov 2006  |  IP: Logged | Report this post to a Moderator
Tincup
Honored Contributor (10K+ posts)
Member # 5829

Icon 7 posted      Profile for Tincup         Edit/Delete Post   Reply With Quote 
TerryK said...

"That's my understanding too. The IDSA denies chronic lyme disease even exists, they call it post lyme and consider it an autoimmune problem.

ILADS is saying there is no evidence that it is an autoimmune problem."

AND... they are using IDSA studies to prove it. Now ain't that a humdinger! Gotta love those guys and gals!

[Big Grin]

Hey shosty...

You said... "So many people with Lyme have negative LP's, and our negative results were, in fact, used against us, not by insurance, but by MD's to validate their position that we have autoimmune problems, and not Lyme."

Actually... insurance companies do use negative LP's against many people. And still they keep it in their criteria (some policies) for evidence of "active infection"... and without a positive LP for Bb.... no treatment..

And... question for you...

You feel Lyme can bring on a case of Lupus.. I am assuming from your posts.

If that is true... what proof does anyone have that Lupus is even a different disease than Lyme and/or coinfections?

Example- If you note the fibromyalgia literature from years back it will show that fibromyalgia was considered the name of a set of symptoms in people who had XYZ similar symptoms. Like Lupus it had no known cause and no known cure.

They are telling people if you have fibromyalgia your body is attacking itself. End of story.

Over the years fibromyalgia "followers" have increased in numbers and gotten worse... and added more symptoms to their original list.

Rather than XYZ symptoms meaning fibromyalgia... now XYZ, RDGC and V symptoms are considered "fibromyalgia.

Same with Lupus and Lyme.

My feeling is they have too much time on their hands.. and Rheumy;s are quite well-known for taking a group of similar symptoms... writing them up... and naming them after themselves. Of course there is never any known cause or cure for them.

If you have a Lyme patient with a list of MANY symptoms like mine.. we could stick me into a half dozen or so of these "autoimmune" categories too.

Then, the only ones who benefit are those who sucker money for themselves for research on how to address the symptoms (not find the cause or cure)... and those who cut costs for insurance by saying nothing works but "more exercise" and anti-depressants (making people not care they are so sick and going down hill)... and/or...

The drug companies profit by making more profits by piece mealing the symptoms and giving a person 8-10 drugs to try to fix each individual symptoms... rather than one drug to address the cause.

Of course then too.. the doctors get more patients and a steady flow of folks that keep coming back for their 5 minute appointments. Cha-ching $$$

Another point...

If you take lots of antibiotics you can expect to develop food allergies due to leaky gut... and this is known to happen. Just so you know.

Anyhow.. would like to hear your thoughts on this theory.

[Big Grin]

--------------------
www.TreatTheBite.com
www.DrJonesKids.org
www.MarylandLyme.org
www.LymeDoc.org

Posts: 20353 | From The Moon | Registered: Jun 2004  |  IP: Logged | Report this post to a Moderator
Shosty
Unregistered


Icon 1 posted            Edit/Delete Post   Reply With Quote 
Parisa, Thanks for the info on IVG and hope your husband continues to benefit.

Tincup, I realize insurance companies use negative LP's against Lyme patients, and still have that in their criteria, but I was just saying that was not what happened to us. I wanted to add that there are other ways a negative LP can affect your care, by increasing the skepticism of other doctors and, in a larger sense, increasing sekpticism about chronic Lyme in general.

I didn't JUST say Lyme can trigger lupus. I tried to say that this is all very murky, and that noone knows much of anything for certain. I laid out the 5 possibilities, for a person with a certain set of symptoms:
-Lyme alone
-illness alone (whatever the cause)
-triggering autoimmunity, with infection still
active
-triggering autoimmunity, with infection
controlled but autoimmunity continuing:
"post Lyme syndrome"
-Lyme and autoimmune illness together, but
existing independent of one another

Regardless of whether Lyme is a specific trigger, some non-mainstream rheumatologists are using antibiotics for autoimmune illnesses. Mycoplasma is another trigger I have read about.

Fibromyalgia sufferers do not have extensive positive autoimmune labs, do they? I'm asking. People throw around the term "autoimmune," but is there clinical evidence of the body attacking itself in fibromyalgia, meaning labs or biopsies?

I am writing about autoimmunity that is proven and meets the mainstream definition of autoimmunity. High anti-nuclear antibody test, skin biopsy, muscle biopsy, anti-DNA and low complements are things we got via labs in our household. Others have more tests than that, which indicate specific autoimmune issues.

I have found that Lymenet rejects the whole concept of autoimmunity, which can be counterproductive for some of us. I also believe in molecular mimicry, since my daughter has insulin-dependent diabetes, triggered by coxsackie. There are people here who say that does not exist,and, even, that Lyme caused my daughter's type 1 diabetes.

Some people have Lyme without the autoimmunity, for whom all this is moot. For those with the HLA-DR4 genetic type,autoimmunity is much more likely with Lyme, a and recovery is harder. Kenneth Ligner writes about this is an article about the "Sensible Pursuit" of answers to Lyme. Dr. Jones was the first one to speak to us about all this. He was the first to test my daughter's ANA, too.

Now, years down the road, my family is off antibiotics, and still sick. We know very well that antibiotics causes leaky gut and food allergies. That is why we are not on antibiotics anymore! People need to know that this is an effect of long-term antibiotics. That is a whole other post.

Our ANA's are high right now. So, is it Lyme or autoimmune problems? I am now looking to confirm lupus for one child, and dermatomyositis or lupus for me, so that we can have other ideas about how to proceed. We cannot take abx. We are doing alternatives with an integrative medicine doctor, but he is also often baffled, as he should be. Certainty of any kind is counterproductive!

Most rheumatologists are hostile to the idea of chronic Lyme. The emotional intensity of this hostility is significant, but so is the emotional intensity that I have seen i some parts of the Lyme community, in opposition to the concept of autoimmunity.

I have written to major and local newspapers begging rheumatologists to open their minds, and to be respectful of different possibilities in a complex picture, concerning Lyme and autoimmunity. I am trying to ask Lyme activists to do the same, because, as things polarize, some of us fall through the cracks.

I can't just jump on the bandwagon and say that my daughter (or I) have Lyme alone. My responsibility is to look at all possibilities, and it is hard.

IP: Logged | Report this post to a Moderator
lou
Frequent Contributor (5K+ posts)
Member # 81

Icon 1 posted      Profile for lou     Send New Private Message       Edit/Delete Post   Reply With Quote 
I personally think that the autoimmune markers in lyme patients are infection driven. How else could you explain symptoms that are improved by abx treatment while having autoimmune markers? Here are two abstracts on the subject, one that shows heavy metals can do this, and cytokines are involved in autoimmunity [as well as infection] and another specifically about lyme and autoimmunity:
----------------------------------------------

Clin Exp Immunol. 2003 Nov;134(2):202-9.

Effects of deviating the Th2-response in murine mercury-induced autoimmunity towards a Th1-response.

Hggqvist B, Hultman P.

Division of Molecular and Immunological Pathology (AIR), Department of Molecular and Clinical Medicine, Linkping University, Linkping, Sweden.

T-helper cells type 1 (Th1) and type 2 (Th2) play an important role in the pathogenesis of autoimmune diseases. In many Th1-dependent autoimmune models, treatment with recombinant interleukin-12 (rIL-12) accelerates the autoimmune response.

Mercury-induced autoimmunity (HgIA) in mice is an H-2 regulated condition with antinucleolar antibodies targeting fibrillarin (ANoA), systemic immune-complex (IC) deposits and transient polyclonal B-cell activation (PBA). HgIA has many characteristics of a Th2 type of reaction, including a strong increase of IgE, but disease induction is critically dependent on the Th1 cytokine IFN-gamma.

The aim of this study was to investigate if a strong deviation of the immune response in HgIA towards Th1 would aggravate HgIA. Injections of both rIL-12 and anti-IL-4 monoclonal antibody (alpha-IL-4) reduced the HgCl2-(Hg-)induced concentration of the Th2-dependent serum IgE and IgG1, but increased the Th1-dependent serum IgG2a. The IgG-ANoA developed earlier and attained a higher titre after combined treatment, and the ANoA titre of the IgG1 isotype decreased while the ANoA titre of the Th1-associated IgG2a, IgG2b and IgG3-ANoA isotypes increased.

Treatment with rIL-12 alone increased the Hg-induced IgG2a and IgG3 ANoA titres, the PBA, and the IC deposits in renal and splenic vessel walls, while treatment with alpha-IL-4 + Hg inhibited renal but not splenic vessel wall IC deposits.

We conclude that manipulating the cytokine status, by altering the Th1/Th2 balance, will influence autoimmune disease manifestations. This might be an important way of modulating human autoimmune diseases.

----------------------------------------------

Infect Immun. 2007 Aug;75(8):3842-7. Epub 2007 May 21.

Pathogen specificity and autoimmunity are distinct features of antigen-driven immune responses in neuroborreliosis.

Kuenzle S, von Bdingen HC, Meier M, Harrer MD, Urich E, Becher B, Goebels N.

Clinical Neuroimmunology Unit, Department of Neurology, University Hospital Zrich, Frauenklinikstrasse 26, CH-8091 Zrich, Switzerland.

Neuroborreliosis (NB) is a chronic infectious disease of the central nervous system (CNS) caused by a tick-borne spirochete, Borrelia burgdorferi.

In addition to direct effects of the causative infectious agent, additional immunity-mediated mechanisms are thought to play a role in the CNS pathology of NB.

In order to further understand the involvement of humoral immune mechanisms in NB, we dissected the intrathecal antibody responses down to the single-plasma-cell level.

Starting with single-cell reverse transcription-PCR of fluorescence-activated cell sorter-sorted cerebrospinal fluid plasma cells from an NB patient, we identified expanded clones and resurrected the antigen specificity of their secreted antibodies through recombinant expression of the correctly paired immunoglobulin heavy- and light-chain genes as monoclonal antibodies (MAbs).

As expected, we found specificity for the causative infectious agent, B. burgdorferi, among the clonally expanded plasma cell (cePC)-derived MAbs.

However, from an independent cePC of the same patient, we could derive MAbs specific for human CNS myelin, without detectable cross-reactivity with B. burgdorferi antigens.

While reactivity against B. burgdorferi is a known feature of humoral immune responses in NB, we show (i) that immune responses specific for self antigens may be a distinct feature of CNS infections independent of pathogen reactivity and (ii) that humoral autoimmunity in NB (since found in cePC) is the result of a truly antigen-driven immune response.

Our findings indicate that in NB mechanisms may be at play that induce distinct immune responses specific for pathogen and self antigens independent from "molecular mimicry."

PMID: 17517881 [PubMed - indexed for MEDLINE]

Posts: 8430 | From Not available | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
lou
Frequent Contributor (5K+ posts)
Member # 81

Icon 1 posted      Profile for lou     Send New Private Message       Edit/Delete Post   Reply With Quote 
And another one:


Infection and Immunity, January 2007, p. 243-251, Vol. 75, No. 1

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

Jan D. Lnemann,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, Charit 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.

* Corresponding author. Mailing address: Institute for Neuroimmunology and Clinical MS Research (INiMS), Center for Molecular Neurobiology Hamburg (ZMNH), University Clinic Eppendorf, Falkenried 94, 20251 Hamburg, Germany.

Published ahead of print on 23 October 2006.

http://iai.asm.org/cgi/content/full/75/1/243

Posts: 8430 | From Not available | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
TerryK
Frequent Contributor (5K+ posts)
Member # 8552

Icon 1 posted      Profile for TerryK     Send New Private Message       Edit/Delete Post   Reply With Quote 
My sister developed lupus while on lyme treatment. I was told that borrelia inserts it's DNA into ours and our immune system attacks us as a result. Apparently this is not uncommon and will likely get better during treatment.

I doubt this is proven yet but certainly seems possible.
Terry

Posts: 6285 | From Oregon | Registered: Jan 2006  |  IP: Logged | Report this post to a Moderator
KS
LymeNet Contributor
Member # 12549

Icon 1 posted      Profile for KS     Send New Private Message       Edit/Delete Post   Reply With Quote 
Shosty,

I totally can appreciate your position and unfortunately, neither side of the fence (ILADS or IDSA) has sufficient scientific data to support any conclusions at this point as to why people don't always get 100% well with long-term treatment. Unfotunately symptoms are not always a sign of active infection. There are just too many variables involved with this disease. We just have to keep an open-mind, keep reading scientific info as it becomes available and trial/error with treatments.

Kristin

Posts: 561 | From mass | Registered: Jul 2007  |  IP: Logged | Report this post to a Moderator
daise
Unregistered


Icon 1 posted            Edit/Delete Post   Reply With Quote 
Hi everyone,

Autoimmune disease has never been proven. It's a theory, cast in concrete back in the '50's--and a mighty weak argument. (As opposed to, for instance, Lyme, which is certainly proven!)

Think of the drug industry profits from marketers surrounding the theory like maggots. Think of the specific drugs for "autoimmune diseases." It's in the best money-interest of these manufacturers to keep flying the flag of "autoimmune disease."

Prescribing Prednisone and the like, which destroys a person's immune system, guarantees sales in painkillers, now and in the future!

There are well over 80 autoimmune diseases. They just keep dumping in more and more illnesses into the autoimmune stew, labeled "autoimmune disease: do not disturb."

I say, enough is enough!

I say no more very mysterious and it's-just-too-hard-to-figure-out-so-we-won't disease.

There just are no significant pure medical science studies into what autoimmune disease is and HOW IT HAPPENS. Yet, our government and some drug makers have poured multimillions into making drugs that target sales to doctors treating autoimmune diseases.

There is no difference between a so-called "autoimmune antibody," and an antibody the body manufactures to fight germs.

They're essentially calling "autoimmune antibodies" an addiction.

I say, when the body sends out it's army of antibodies to fight serious illness, it is straightforward that they often need to try to get inside cells, where the germs are! But our bodies have not evolved for the antibodies to be able to get inside cells--at least not with their "instructions" to go after Lyme, etc.

The ducks say germs can't get inside cells. We all know differently. Heck, even cancer gets inside cells. Dumb Ducks. Quack! But it feeds their paychecks and makes rich some drug makers.

I say autoimmune disease is not caused by the mysterious boogyman, it is caused by pathogens, plain and simple. Occams razor!

Further, I think we of Lymeland will eventually cut a swath across corporate America and crooked politicians and we Lymies will save the day! America--nor the world--will never be the same.

However, I think autoimmunity is possible in a small number of patients. Anything is possible.

daise [Smile]

[ 16. June 2008, 05:10 PM: Message edited by: daise ]

IP: Logged | Report this post to a Moderator
Greatcod
Unregistered


Icon 1 posted            Edit/Delete Post   Reply With Quote 
Kristin wrote "Unfotunately symptoms are not always a sign of active infection."

This is something I have become very curious about.
What are some of the other illnesses where symptoms continue after the pathogen is eradicated?
I can see the problem where perhaps tissues are so damaged from the infection that symptoms continue after the pathogen is eliminated, but I don't know enough medicine to know what any of those illnesses are.
Thanks.

IP: Logged | Report this post to a Moderator
Shosty
Unregistered


Icon 1 posted            Edit/Delete Post   Reply With Quote 
Wow, there is a lot of info in the last few posts! KS, well said., better than I could write.

Lou, that is all great info. Right now, I guess I would say that I tried to cover all scenarios, and the studies you posted do confirm that Lyme and other pathogens can trigger autoimmunity. I think that is something everyone agrees on.

Detoxifying heavy metals is one of the many other avenues, besides abx, that people are pursuing (this is referred to on this forum quite a bit). This would be another scenario that I tried to include, autoimmunity that is not triggered by Lyme, but something else.

I am trying to say that I do not know, that these things are fuzzy, and that all those 5 scenarios are possible, in combination or alone.

I have no doubt that molecular mimicry exists, since my daughter has lived with type 1 diabetes ever since she had coxsackie at age 4.But noone has said that this causes Lyme, have they?

Type 1 diabetes and heart problems from rheumatic fever are examples of illnesses that continue once the pathogen is eradicated. It is possible that lupus and MS and other autoimmune illnesses also continue after the pathogen is eradicated, although, with Lyme, and its ways of evading destruction, I certainly have my doubts about whether this could happen with Bb. And, as I said, some MD's feel that abx help other illnesses in this category.

There is some confusion about what autoimmunity is, I think. Antinuclear antibodies and anti-DNA antibodies are NOT the "regular" antibodies produced when there is a bug to fight. In fact,taking echinacea or other meds to stoke the immune system can HURT people who have autoimmune stuff going on,because they strengthen the attack against self. Meds like Plaquneil and prednisone do the opposite: they tamp down the immune system, and that is why steroids make Lyme worse.

For those of you who do not have positive ANA's and anti-DNA's and skin biopsies and so on, that tell you that you have autoimmune disorders, this debate is probably not all that meaningful. But in my household, Lyme reatment did NOT change our autoimmune markers. We have positive Lyme Western Blots, but also positive labs for autoimmune problems. We have no idea which came first, and there is no way to tell if our Lyme is gone. We do know that the autoimmune problems are still here.

This is a mystery that plagues many people with many problems. This is not to say, let's give up, and toss it in the autoimmune trash can.

I am just saying that so many MD's, researchers and patients are caught up in the controversy about chronic Lyme versus post-Lyme autoimmune disease, and the debate is so polarized, that I think some of us lose out.

As soon as I mention Lyme to certain MD's, they get a look in their eyes. But, if I mention autoimmunity, the same thing happens with a Lyme group.

I am trying to live with uncertainty and do the best I can for my family, covering all bases and keeping an open mind.

IP: Logged | Report this post to a Moderator
hcconn22
LymeNet Contributor
Member # 5263

Icon 1 posted      Profile for hcconn22   Author's Homepage     Send New Private Message       Edit/Delete Post   Reply With Quote 
You know ya gotta look at the RESULTS.

Alan Steere first thought Lyme was a virus

1 --- HE WAS DEAD WRONG

The he and his team were involved in Lymerix vaccine.

2 --- THE VACCINE FAILED BIG TIME.

Next he says it's Autoimmune Disease
With all the $$ and support;

3 --- HE CAN NOT PROVE IT OR EVEN COME CLOSE.

In business it's all about outcomes/results. From the best I can tell he has produced papers and scientific studies, and may be a good salesperson for his ideas;

4 --- BUT NO/ NADA RESULTS.

It's about time that the CDC, NIH, Pharma and others start looking at Results and what they have gotten in the past for all their millions in dollars in grant money.

You could also add IDSA Guidelines

and Deerborn Test Standards to his Resume........

Starts looking real bad if you ask me.

--------------------
Positive 10 bands WB IGG & IGM
+ Babesia + Bartonolla and NOW RMSF 3/5/09 all at Quest

And still positive ELISA and WB two years after IV treatment
http://www.lymefriends.org/profile/blake

Posts: 607 | From Tick Town, Connecticut | Registered: Feb 2004  |  IP: Logged | Report this post to a Moderator
ssmillik
Member
Member # 9635

Icon 1 posted      Profile for ssmillik     Send New Private Message       Edit/Delete Post   Reply With Quote 
Is autoimmunity something that doesn't go away even with antibiotic treatment? If so, I have Addison's disease (autoimmune) as a result of Lyme. Even though I'm symptom-free of Lyme, my Addison's is here to stay. In fact, it wasn't until I started getting treated for Addison's disease that I started getting better from Lyme.

I do believe autoimmune disease comes from some sort of stressor, be it an infection or some physical trauma, but you can't get rid of every autoimmune disease with antibiotics.

Posts: 39 | From Massachusetts | Registered: Jul 2006  |  IP: Logged | Report this post to a Moderator
lou
Frequent Contributor (5K+ posts)
Member # 81

Icon 1 posted      Profile for lou     Send New Private Message       Edit/Delete Post   Reply With Quote 
That is the big question. Infection produces autoimmune markers, but do they stay after the infection is gone, causing disease by themselves? No one seems to doing the tests to see if the markers leave when the infection is successfully treated.

This is why we need research money, and need for it to be answering key questions like this. NIH money is now funding the bumsteere, who cannot see the elephant in the room and never changes his mind no matter how much evidence contradicts his opinions. We need honest unbiased research, which NIH has never funded on the key questions, or if they have funded the studies, they choose the recipients with a predetermined outcome in mind.

Posts: 8430 | From Not available | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
Shosty
Unregistered


Icon 1 posted            Edit/Delete Post   Reply With Quote 
For more on this whole topic, please look at the post above, on the "gene that makes Lyme hard to treat." There is a list of genetic types for whom Lyme is "refractory," or, for some, antibiotics are ineffective, due to this genetic predisposition to autoimmunity. A majority of people with longer term Lyme arthritis, had two HLA genetic types, as compared to people without.

Again, Ligner writes well on this.

I think the real question is, can we ever know if the infection has been eradicated?

We (our family members) still have autoimmune markers after all these years of Lyme treatment. Some symptoms are lessened or even gone, but others are still here, or even worse.

There is no way to know whether we should be on antibiotics, or be treating autoimmune problems, or both. Objective research is definitely needed, but there is really no way to do it until there is a way to tell whether the Lyme is "cured," dormant, or still active.

Markers for autoimmunity are easy to measure. Some of them cross-react with Lyme tests, though, and vice-versa, making things even more confusing.

I don't mean to keep repeating myself. But the main difference I have with Steere et al isn't the idea of continuing autoimmunity, it is with the length of time he/they recommend for antibiotics.

That said, antibiotics HAVE done us a lot of harm. Necessary harm perhaps, I don't really know.

IP: Logged | Report this post to a Moderator
lou
Frequent Contributor (5K+ posts)
Member # 81

Icon 1 posted      Profile for lou     Send New Private Message       Edit/Delete Post   Reply With Quote 
I am very suspicious of genetic explanations for disease. They are used too often.

There is also the possibility of microbes affecting gene expression, which is another thing entirely. If you are interested in this, read up on epigenetics.

Posts: 8430 | From Not available | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
   

Quick Reply
Message:

HTML is not enabled.
UBB Code is enabled.

Instant Graemlins
   


Post New Topic  New Poll  Post A Reply Close Topic   Feature Topic   Move Topic   Delete Topic next oldest topic   next newest topic
 - Printer-friendly view of this topic
Hop To:


Contact Us | LymeNet home page | Privacy Statement

Powered by UBB.classic™ 6.7.3


The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:

The Lyme Disease Network of New Jersey
907 Pebble Creek Court, Pennington, NJ 08534 USA


| Flash Discussion | Support Groups | On-Line Library
Legal Resources | Medical Abstracts | Newsletter | Books
Pictures | Site Search | Links | Help/Questions
About LymeNet | Contact Us

© 1993-2020 The Lyme Disease Network of New Jersey, Inc.
All Rights Reserved.
Use of the LymeNet Site is subject to Terms and Conditions.