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» LymeNet Flash » Questions and Discussion » Medical Questions » Lyme Disease The Role of Autoimmune Reactivity

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Author Topic: Lyme Disease The Role of Autoimmune Reactivity
soonermom
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http://tinyurl.com/rxgulz

I WISH I lived in Maryland so I could participate!!


I know some of this isn't new information, but I was surprised to see it on an NIH website.



Lyme Disease

The Role of Autoimmune Reactivity

The results of recent studies conducted by NIAID and intramural scientists from the National Institute of Neurological Disorders and Stroke (NINDS) indicate that T cells from patients with chronic Lyme disease are reactive not only against B. burgdorferi-specific antigens but also against various host (self) antigens (Nature Medicine 5: 1375, 1999).

Such antigenic mimicry might generate autoimmune inflammatory reactions that could be responsible for arthritic as well as some neurological symptoms associated with chronic Lyme disease.

Intramural and extramural scientists are exploring the implications of this finding.

Antibodies against the OspA epitopes of B. burgdorferi also have been shown to cross react with neural tissue (J. Peripheral NervousSystem 9, 165, 2004; J Neuroimmunol 159, 192, 2005) as well as myocin (J Clin Microbiol 43, 850, 2005).

Such antigenic mimicry may have the potential to generate autoimmune inflammatory reactions that could be responsible for the neurological symptoms associated with chronic Lyme disease.

Intramural and extramural scientists are evaluating this possibility in greater detail.

In this context, it is interesting to note that homologies between proteins of B. burgdorferi and thyroid antigens also have been reported (Thyroid 14, 964, 2004).

In clinical studies conducted by NIAID-supported extramural scientists, case subject patients with post-treatment chronic Lyme disease (PTCLD) were compared to control subjects without such symptoms for the presence of several human leukocyte antigen (HLA) class II (DRB1 and DQB1) genetic markers, some of which are known to be associated with the expression of autoimmune reactivity.

The results obtained did not support the involvement of an autoimmune mechanism in PTCLD (J Infect Dis :192, 1010, 2005) .

However, since not all autoimmune diseases are associated with specific HLA haplotypes, these findings do not necessarily exclude that possibility.

Definitive proof clearly would involve demonstrating the presence of significant levels of relevant autoimmune antibodies and/or autoreactive T cells in patients with PTCLD but not in treated control subjects without such symptoms.

A greater frequency of DRB1*0401, which has been reported to be associated with antibiotic-treatment resistant arthritis (Science 281: 703, 1998) was noted in the case subject patients; although this finding appeared to be nominally significant (p < 0.05), its biological significance is ambiguous since none of the case subjects considered had symptoms of inflammatory arthritis.

--------------------
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bettyg
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buried on page 2; up for those not getting a chance to read this..
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Shosty
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Why are you surprised?

This article supports the idea that Lyme may trigger an autoimmune "post-Lyme" condition involving arthritis and neurological symptoms.

It is not saying that chronic Lyme involves continuing infection, and does not say that long-term treatment with antibiotics will be useful.

Molecular mimicry continues when the pathogen is gone, and is an autoimmune process, not an infectious one.

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lou
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This has been their contention all along, that post lyme syndrome is autoimmune, not infectious. So then they treat it with steroids or something else, not abx. It ignores the studies that show spirochetes still around in animals and humans after what was supposed to be curative abx treatment.

However, autoimmunity can be driven by ongoing infection. Maybe it always is, and they just are too short sighted to see it. Look at all the conditions that are now said to be autoimmune. The new trash can diagnosis.

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Bugg
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Thanks for posting this info....
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nenet
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Thank you, that was interesting especially the conclusions of their study:

"In clinical studies conducted by NIAID-supported extramural scientists, case subject patients with post-treatment chronic Lyme disease (PTCLD) were compared to control subjects without such symptoms for the presence of several human leukocyte antigen (HLA) class II (DRB1 and DQB1) genetic markers, some of which are known to be associated with the expression of autoimmune reactivity.

The results obtained did not support the involvement of an autoimmune mechanism in PTCLD(J Infect Dis :192, 1010, 2005)."

--------------------
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jentytib
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I could enter the above study. Should I? Will it screw me over somehow??

I'll be in MD for 2 months this summer.

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nenet
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I must be missing something -

where does it say there is a current study being planned?

I wouldn't put it past me to miss something blatantly obvious, but as far as I can tell, the link provided only described results of recently completed studies, and nothing about any new studies in the works.

Can someone help me out here?

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Dr. C's Western Blot Explanation

Lymenet Success Stories

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Medical & Scientific Literature on Lyme

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soonermom
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If you click on the link and then look to the right there is a big orange button that says volunteer for clinical studies. If you click on that it pulls up all the studies related to lyme disease.

I believe all autoimmune diseases are triggered by an initial infection. It's one thing to fight an active infection, but if your own immune system has turned on you......that is a whole other issue.

I am definitely NOT one to dispute the obvious long term infections that many of us experience. I do have my own concerns; however, about the autoimmune aspect of the antibody for OspA. I recently found out that I have 3 more brain lesions (16 total now) after almost a year of treatment for lyme. You can see below what my WB showed in regards to the antibody for OspA (band 31).

It is possible that the changes in my MRI were due to the infection. I will probably never know for sure.

"Cure Unknown" speaks on this topic and how some LLMD's are using IVIG for an autoimmune peripheral nervous system disease triggered by lyme.

I don't see why you can't believe in both aspects of this bacteria?

--------------------
3/08 CDC Positive
IgM 18++ 23-25IND 31++++ 34++ 39+ 41+++ 58+ 83-93+

CDC Negative
IgG 31IND 39IND 41+++ 58+ 66+

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nenet
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quote:
Originally posted by soonermom:
If you click on the link and then look to the right there is a big orange button that says volunteer for clinical studies. If you click on that it pulls up all the studies related to lyme disease.

Thanks for helping me there!

For those who also might have trouble finding it, this trial looks like it is addressing questions of possible persistence of infection vs possible post-Lyme treatment autoimmune issues:

"Evaluation of Lyme Disease: Clinical, Microbiological and Immunological Characteristics"

http://clinicaltrials.gov/ct2/show/NCT00001539?term=Lyme+Disease+and+NIAID&recr=Open&rank=2

"This study will determine whether patients who have been infected with the Lyme bacteria, Borrelia burgdorferi, and treated with antibiotics still have the bacteria alive inside them and whether it is causing their symptoms.

The information from this study may serve as a basis for developing stringent diagnostic criteria for Lyme disease and the establishment of future treatment trials."


quote:
Originally posted by soonermom:
I believe all autoimmune diseases are triggered by an initial infection. It's one thing to fight an active infection, but if your own immune system has turned on you......that is a whole other issue.

I am definitely NOT one to dispute the obvious long term infections that many of us experience. I do have my own concerns; however, about the autoimmune aspect of the antibody for OspA. I recently found out that I have 3 more brain lesions (16 total now) after almost a year of treatment for lyme. You can see below what my WB showed in regards to the antibody for OspA (band 31).

It is possible that the changes in my MRI were due to the infection. I will probably never know for sure.

"Cure Unknown" speaks on this topic and how some LLMD's are using IVIG for an autoimmune peripheral nervous system disease triggered by lyme.

I don't see why you can't believe in both aspects of this bacteria?

I don't think I ever stated a belief or judgement one way or the other in relation to whether Lyme can cause autoimmune problems. I am only interested in what the science can provide, so that we can all get better.

Perhaps you were asking that question to someone else? I'm a little slow today, so please forgive any confusion on my part. Serious brain fog (almost spelled that "gof").

--------------------
Dr. C's Western Blot Explanation

Lymenet Success Stories

ILADS Treatment Guidelines

Medical & Scientific Literature on Lyme

"Long-Term Antibiotic Therapy Improves Persistent Symptoms Associated with Lyme Disease"

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Richard1062
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What does cross react mean?

As in, "antibodies against OSP A have been show to cross react with neural tissue"

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