Fw: Reprogramming the Immune System -- Article from MSNBC.com

[Guest guest]

> Reprogramming the immune system

>

> Approach uses the body's own cells to fight multiple sclerosis

> In multiple sclerosis, immune-system cells called T cells attack and

> damage the myelin sheath that protects nerve cells, or neurons.

>

>

> By Charlene Laino

> MSNBC

>

> Jan. 23 - It's like pouring gasoline on a fire to put it out. Yes,

> you read correctly: that's the best way to describe a novel approach

> that shows promise for treating multiple sclerosis using an extremely

> large dose of the very substance that is causing the disease to begin

> with.

> FOR THE first time, scientists have shown that the

> experimental approach works in non-human primates with multiple

> sclerosis. And there's every reason to believe, they say, that the

> same tactic could help stomp out symptoms in humans suffering not only

> from MS, but also from other autoimmune diseases, such as rheumatoid

> arthritis to diabetes.

> The feat is the latest to grow out of a new molecular-level

> understanding of autoimmune diseases, the umbrella term for some

> 40-plus conditions in which the body's immune system - its first line

> of defense against foreign invaders - runs amok.

> Researchers have known for years that autoimmune diseases

> result when a malfunctioning immune system mistakenly recognizes

> certain cells in the body as the enemy and launches an all-out attack.

> In multiple sclerosis, the myelin sheath - the protective covering

> that surrounds nerve cells in the brain and spinal cord - is the

> target.

> More recently, experiment showed that specialized immune-system

> cells called T-helper cells are the key players, the culprits that

> produce substances that attack and damage the myelin sheath. The

> result is devastating for the millions of Americans with the disease:

> fatigue, dim or blurred vision, disturbed speech, memory loss, muscle

> weakness, even paralysis. The " lucky " ones merely suffer mild weakness

> for decades (though always wondering if their condition will worsen);

> others steadily deteriorate from repeated attacks.

> Meanwhile, scientists were gaining a better understanding of a

> well-honed immune system - a system in which the same T cells that

> wreak havoc in MS are gallant warriors. It became clear that like

> soldiers, T-helper cells sit ready for invasion from a foreign

> invader, be it a flu bug, food-borne bacteria or other pathogen. Then,

> as soon as they recognize the enemy, these T cells turn into

> commanding officers of sorts and begin multiplying until an entire

> army is set to fight.

> " But like any potent weapon, you want to control how much is

> deployed, " says the National Institutes of Health's Dr.

> Lenardo. " If the cells just kept multiplying ... you'd have a surfeit

> of T cells, very potent activators that can actually kill you - as

> happens in toxic shock syndrome. "

>

> PROGRAMMED FOR DESTRUCTION

> Fortunately, every cell has a built-in suicide mechanism. " When

> there are too many soldiers, they are programmed to self-destruct, " he

> says. " A healthy immune system doesn't let your T cells grow

> uncontrolled and kill you. "

> Several years ago, Lenardo, a researcher at the National

> Institute of Allergy and Infectious Diseases' laboratory of

> immunology, decided to put the new knowledge about the immune system

> in general and MS in particular to a test. Since MS is an autoimmune

> disease in which T-helper cells are activated that shouldn't be,

> Lenardo reasoned that he could thwart the disease if he could just

> activate T-helper cells' built-in suicide mechanism.

> Working at first in the lab, Lenardo proved his point. As

> expected, T-helper cells exposed to small amounts of the proteins

> making up the myelin sheaths were stimulated to attack the sheaths.

> But, paradoxically, when these activated T-helper cells were

> exposed to large amounts of the same proteins, they died off. " Instead

> of robust proliferation, which is what we expected, we got

> self-destruction, " says Lenardo. " We observed negative feedback. "

> Advertisement

>

>

> Next, Lenardo tried the experiments in mice, " with very

> dramatic results. Not only did the MS mice become healthy, but the

> disease-causing T cells were actually eliminated, " he says.

>

> MONKEY BUSINESS

> In the latest test, nine male marmoset monkeys were injected

> with just enough myelin proteins to stimulate their T cells to attack

> myelin sheaths, inducing a disease very similar to MS in humans. Three

> monkeys then received additional large doses of myelin proteins, three

> got moderate doses, and three received nothing.

> About three months later, all three of the untreated monkeys

> showed symptoms of the disease. In contrast, none of the primates who

> got large doses of myelin had symptoms. The moderate-dose group didn't

> fare as well, with two showing symptoms, though less severe ones than

> their untreated counterparts. The report appears in the February issue

> of the Journal of Immunology.

> Imaging scans of the animals' brains further validated the

> observations. Magnetic resonance images revealed severe damage to the

> myelin sheaths in two of the untreated monkeys and one of the

> moderate-dose monkeys. Minor damage did occur in the large-dose group,

> indicating the disease process had not been completely thwarted

> although it had been greatly suppressed, Lenardo says.

> " They've re-educated an immune system gone awry, " says Dr.

> O'Looney, director of biomedical research at the National

> Multiple Sclerosis Society in New York. " This certainly holds great

> promise. "

> One of the most exciting aspects of the new work is that it

> marshals the body's own, nontoxic resources to fight off the disease.

> Similar to chemotherapy for cancer, current treatments for MS and

> other autoimmune diseases are atom bombs of sorts, killing or

> suppressing everything in their wake, good or bad.

> " Conceptually, we have a very powerful new tool, " Lenardo says.

> " It selectively homes in only on those cells causing the disease

> rather than shutting down the entire immune system. "

> There are even advantages over other immune-based approaches to

> autoimmune diseases, he says. " The others just paralyze T cells, but

> they could wake back up. This actually gets rid of them. "

> With human testing still on the horizon, it's too early to say

> whether Lenardo's approach is best. But with one in 20 Americans

> victim of one autoimmune disease or another, at enormous personal cost

> in pain and suffering and at monetary costs topping $100 billion each

> year, it's certainly worth a shot.

>

> from: http://www.msnbc.com/news/520601.asp

[Guest guest]

Is this not the same old nonsense?

>

> To unsubscribe, email: rheumatic-unsubscribeegroups

>

>

[Guest guest]

> Is this not the same old nonsense?

>

Not by my interpretation. Many doctors believe that even if RA is

triggered by infections, that once the autoimmune process is started, the

reaction rolls, despite removing the infectious trigger. So personally, I

found it interesting and relevant. Particularly keeping in mind the recent

research regarding t-cells in RA from Cornelia Weyand et al. Your views on

it seem to be different, so I would appreciate hearing them, if you want to

share why you think it is nonsense. Liz G.

[Guest guest]

Hi Liz (and all) :-)

I'm not a doctor. I'm not a scientist. And my thinking may sound

simplistic, but here it goes.....

Many people in this group, at The Road Back Foundation, former patients of

Dr. Brown, of Dr. Franco, of Dr. Chiu, etc. (myself included) have treated

the underlying infection and have regained their health. If the disease

process was simply " triggered " by infection and carried on by the autoimmune

process, why is this so? Why does the antibiotic treatment work? Why do we

not have to suppress the immune system to stop the autoimmune process?

I thought that the whole idea behind this treatment was that the immune

system was actually depressed, allowing the infection to take-hold, and that

the immune system is trying to fight the " invader " and not the person's

tissues.

I agree with you that many, many doctors (most, probably) believe that these

diseases are " autoimmune " . And many admit that there may be some unknown

trigger that " starts the process " . I admit that my ideas go against

conventional medical wisdom. But am I way out in left-field here? Are my

thoughts not shared by others in this group? I thought that these beliefs

about the disease process were the basis of the rheumatic.org website, etc.

Please be kind and don't butcher me with your responses. :-)

Feeling great and loving my t-cells.....

Re: rheumatic Fw: " Reprogramming the Immune System " -- Article

from MSNBC.com

>

>

> > Is this not the same old nonsense?

> >

>

> Not by my interpretation. Many doctors believe that even if RA is

> triggered by infections, that once the autoimmune process is started, the

> reaction rolls, despite removing the infectious trigger. So personally, I

> found it interesting and relevant. Particularly keeping in mind the

recent

> research regarding t-cells in RA from Cornelia Weyand et al. Your views

on

> it seem to be different, so I would appreciate hearing them, if you want

to

> share why you think it is nonsense. Liz G.

>

>

> To unsubscribe, email: rheumatic-unsubscribeegroups

>

>

[Guest guest]

HI all,

On Thursday 25 January 2001 06:06, you wrote:

} Hi Liz (and all) :-)

}

} I'm not a doctor. I'm not a scientist. And my thinking may sound

} simplistic, but here it goes.....

I'm not a (medical) doctor, but I am a scientist of sorts. However, this

isn't really my field.... (in other words, I'm no authority on this, so you

don't have to take any notice of me! :-) )

} Many people in this group, at The Road Back Foundation, former patients of

} Dr. Brown, of Dr. Franco, of Dr. Chiu, etc. (myself included) have treated

} the underlying infection and have regained their health. If the disease

} process was simply " triggered " by infection and carried on by the

} autoimmune process, why is this so?

Because the trigger sets off a response from the T cells to a particular

protein. That protein happens, through a process called molecular mimicry, to

be extremely similar to a protein of your own tissues. There are many

different tissue types, but people with RA are predominantly HLA-DR1 and

HLA-DR4. Ankylosing spondylitis is HLA-B27, and I expect other types go for

other conditions.

So, you have an infection, which has started off the T-cells. And as long as

the infection is there, the T-cells are producing antibodies to attack the

infection, but those same antibodies will also attack your own tissue.

} Why does the antibiotic treatment work?

Because if you get rid of the infection, the T-cells will no longer need to

produce antibodies to it.

} Why do we not have to suppress the immune system to stop the

} autoimmune process?

We're only suppressing the response to one particular protein (a protein that

is unique to the infectious agent, but very similar to one in your own

tissue) in this instance. That might, or might not, be important, depending

on what the cause of the infection, or response, is. For example, the

response could be due to a by-product of a bacterial infection, not the

bacteria itself, in which case it is perfectly safe to prevent the body

reacting to that by-product.

} I thought that the whole idea behind this treatment was that the immune

} system was actually depressed, allowing the infection to take-hold, and

} that the immune system is trying to fight the " invader " and not the

} person's tissues.

The beauty of this method is that it only suppresses the immune response to

one particular protein, so apart from that, the immune system will continue

as usual.

It may well also be the case that once an immune response has been triggered,

it is not sufficient to get rid of the infection causing it. The T-cells that

have been trained to respond to the infection may continue to produce some

antibodies, and cause inflammation by molecular mimicry - I don't know.

I may be way off here, but when I read the article posted by Liz, I thoughtit

held a lot of promise. It may need to be administered in conjunction with

antibiotics; indeed this would seem a very good method. Kill the infection

using antibiotics, whilst also getting rid of the body's own antibodies to

the particular infection (just rely on the antibiotics to do it for you).

That way, you will be pain-free much quicker.

In short, I think this is a promising new development, and is not at all

similar to the " wipe out all T-cells " approach that has been proposed

recently. But time will tell.

Regards,

--

D. Shaw

Sefydliad y Gwyddorau Biolegol

Prifysgol Cymru

Aberystwyth, Cymru

[Guest guest]

I personally thought the article was fascinating. I am ready for them to

try it on some brave souls, so we all can get out of this pickle eventually.

Thanks for your research and keep it coming.

Gloria

[Guest guest]

Hi (and everyone).

I don't mean to be argumentative here. I'm certainly no authority. In

fact, my brain is feeling pretty scrambled! :-( I've left some of our

earlier conversation quoted below. Please, (or SOMEone that can help

clarify).....I'm confused. I, of course, think it's a step in the right

direction that doctors/scientists are concerned with the old overall immune

system suppression. But what I don't get is this: If our goal is to

completely get rid of the infection, isn't it counter-productive to kill off

the very t-cells that are targeting that infection? I was recently told

that, although I'm dramatically improved, the minocin will never kill off

ALL of the mycoplasma and I need to continue to build UP my immune system to

get rid of those last buggers.

Am I making any sense? Help my tired brain, please! :-)

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

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

> } Why does the antibiotic treatment work?

>

> Because if you get rid of the infection, the T-cells will no longer need

to

> produce antibodies to it.

>

> } Why do we not have to suppress the immune system to stop the

> } autoimmune process?

>

> We're only suppressing the response to one particular protein (a protein

that

> is unique to the infectious agent, but very similar to one in your own

> tissue) in this instance. That might, or might not, be important,

depending

> on what the cause of the infection, or response, is. For example, the

> response could be due to a by-product of a bacterial infection, not the

> bacteria itself, in which case it is perfectly safe to prevent the body

> reacting to that by-product.

>

> } I thought that the whole idea behind this treatment was that the immune

> } system was actually depressed, allowing the infection to take-hold, and

> } that the immune system is trying to fight the " invader " and not the

> } person's tissues.

>

> The beauty of this method is that it only suppresses the immune response

to

> one particular protein, so apart from that, the immune system will

continue

> as usual.

> --

[Guest guest]

Thank you , You said exactly what was going through my mind when I

read this. When I saw this article, it was like I heard a big " click " in my

mind and another piece of the most complicated mother-loving puzzle I've

ever tried to sort out (RA) fell into place.

Think, why do some perfectly healthy people have mcyoplasmas and other

chronic infections and not get arthritis from it? It comes down to the

genetic predisposition on the histocompatibility genes (the HLAs

referred to) Molecular mimicry, and reactive arthritis. Collateral damage

while waiting for the PA to work and herxing. Rebalancing and Rebuilding a

healthy immune system when it has been skewed to confuse self with non-self

(mycoplasma or other trigger). Just listing some of the puzzle pieces. I'd

hate to think that I got rid of my infections, only to have the process roll

on. Remember, not everyone is positive for the HLAs, so it might not apply

to all. I've not been tested for HLA, but feel I probably am positive,

since RA and other " autoimmune " diseases run in both sides of my family.

It was especially promising to me since I cannot take immune boosters like

echinacea without going into the mother of all flares after a few days.

Cranks up those self-targeted T cells along with the rest. This seems to be

one potential method, if it pans out, of correcting the immune system by

invoking it's own checks and balances system, like screaming " SELF " at it

with the proteins so they will say " Our work is done for now " . It does not

wipe them out, it just telIs the to " chill out " , if I'm interpreting it

correctly. I wonder if this has anything to do with why type2 collagen

works. It will be exciting to see what comes of this.

Thanks for putting it clearly, , I hope I haven't gone back and

muddied the waters with my own version. LOL I'm in a state right now,

recovering from a long wait to have a dying tooth removed (it's out, as of

yesterday, yippee!--another story), and also recovering from an awful

bladder infection. Maybe my tooth wouldn't heal and my bladder got infected

because my immune system was too busy trying to rip the hell out of my

joints?? Take care, all, Liz G.

[Guest guest]

Re: rheumatic Fw: " Reprogramming the Immune System " -- Article

from MSNBC.com

> Think, why do some perfectly healthy people have mcyoplasmas and other

> chronic infections and not get arthritis from it?

Is this true? Are there perfectly healthy people walking around with

chronic mycoplasma infections? Do we know this? Or do they have one or

more of the many " autoimmune " diseases? Or perhaps when " normal, healthy "

people come in contact with mycoplasma (or other infectious agents) their

normal, healthy immune systems simply fight it off and, thus, they remain

normal and healthy?

It comes down to the genetic predisposition on the histocompatibility genes

(the HLAs

> referred to) Molecular mimicry, and reactive arthritis. Collateral

damage

> while waiting for the PA to work and herxing. Rebalancing and Rebuilding

a

> healthy immune system when it has been skewed to confuse self with

non-self

> (mycoplasma or other trigger). Just listing some of the puzzle pieces.

I'd

> hate to think that I got rid of my infections, only to have the process

roll

> on. Remember, not everyone is positive for the HLAs, so it might not

apply

> to all. I've not been tested for HLA, but feel I probably am positive,

> since RA and other " autoimmune " diseases run in both sides of my family.

>

>

>

[Guest guest]

> Is this true? Are there perfectly healthy people walking around with

> chronic mycoplasma infections? Do we know this? Or do they have one or

> more of the many " autoimmune " diseases? Or perhaps when " normal, healthy "

> people come in contact with mycoplasma (or other infectious agents) their

> normal, healthy immune systems simply fight it off and, thus, they remain

> normal and healthy?

I was basing my comment on this:

~~~~~~~~~

Autoimmune Illnesses

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

----

Prof. Garth L. Nicolson

Rheumatoid Arthritis, Multiple Sclerosis, Amyotrophic Lateral Sclerosis,

Inflammatory Bowel Diseases, Scleroderma and other Autoimmune Diseases

Autoimmune Diseases are complex, multiorgan diseases of unknown etiology.

Although we do not know exactly what causes Autoimmune Diseases, there is

increasing evidence that in many patients chronic infections, particularly

by certain bacteria and viruses, play an important role in these diseases

along with genetic predisposition and immune dysfunction. How could

infections be important in Autoimmune Diseases? They could be involved in

helping to cause the illness, or they can affect patients by serving as

cofactors for the illness (not causing illness on their own but serving as

important factors in the disease process) or even as opportunistic

infections that increase patient morbidity (sickness) and complications

associated with the disease (see Nicolson et al., Antimicrobics and

Infectious Diseases Newsletter, 1999).

Infections have been found in a variety of Autoimmune Diseases, particularly

in Rheumatic Diseases, such as Rheumatoid Arthritis, Scleroderma, and other

rheumatic disorders. We and others have gathered substantial evidence that

chronic bacterial and viral infections are commonly associated with

Rheumatic Diseases, and many of these patients respond to antibiotic

therapy. These patients are now recovering from their illnesses after

decades of inadequate diagnoses and treatments. The recovery is slow; it

usually takes up to or over a year to recover, but these patients had no

alternative or effective treatments for their conditions, other than the

alleviation of pain.

Neurological Autoimmune Diseases

We and others have also found chronic infections in a variety of autoimmune

neurologic diseases, such as MS, ALS, Lupus (SLE), among others. We

previously proposed that many and perhaps a majority of these patients might

be suffering from mycoplasmal and other infections that can cause, in part,

their complex signs and symptoms. Systemic chronic infections (caused by

bacteria such as Mycoplasma, Chlamydia, Borrelia, Brucella, etc. or viruses

such as CMV, HHV6, EV or enterovirus, etc.) can dysfunctional immune

responses and in extreme cases autoimmune-like disorders. Microorganisms

like mycoplasmas can invade virtually every human tissue and can compromise

the immune system, permitting opportunistic infections by other bacteria,

viruses, fungi and yeast.

When mycoplasmas exit certain cells, such as synovial cells, nerve cells,

among others that can be infected, they can stimulate autoimmune response.

This can occur by different mechanisms. One mechanism that has intrigued us

is that when certain microorganisms, such as certain species of mycoplasmas,

exit from invaded cells, they carry part of the host cell membrane on their

surface. This may trigger the immune system to respond to the host antigens

on the foreign microorganism. Alternatively, some microorganisms display

surface antigens that mimic host cell surface antigens, and these may

stimulate autoimmune responses.

Other Autoimmune Diseases

Our recently published studies demonstrated a possible link between

mycoplasmal infections and Rheumatoid Arthritis, since we found high

frequency of multiple mycoplasmal infections in these patients (Haier et

al., 1999). Previously we examined a variety of patients with chronic

illnesses for the presence of mycoplasmal infections. We found that about

one half other autoimmune diseases (Inflammatory Bowel Diseases, Sjögren's,

Hashimoto's, Graves', Reiter's, Crohn's Diseases and others) are also

associated with mycoplasmal, chlamydial, and other infections. Although

these diseases have not been treated with antibiotics in large, blinded

trials, there is some anecdotal evidence that antibiotics can be effective

in a program with other treatments to alleviate morbidity in these patients.

New Treatments for Autoimmune Diseases

Patients with 'stealth' infections, such as caused by mycoplasmal and other

bacteria, can be treated using antibiotics effective against such

infections, and once they recover, their blood is no longer positive for the

presence of the infection. Recent double-blind clinical studies sponsored by

the National Institutes of Health indicate that some antibiotics are

effective in treating Rheumatoid Arthritis. Our recent results indicate that

in addition to Rheumatoid Arthritis other autoimmune diseases can be treated

with antibiotics to suppress chronic bacterial infections, and antivirals to

suppress chronic viral infections. Patients with such infections gain

significant clinical benefits by undergoing therapies against chronic

bacterial and viral infections.

For information about the clinical testing for mycoplasmal, chlamydia,

viral, and other chronic infections see Clinical Testing or International

Molecular Diagnostics.

~~~~~~~~~~~~~~~

and this: long, so I'm posting the link and a quote

http://www.immed.org/publications/autoimmune_illness/apr2.html

Results

For the detection of mycoplasmal infections in blood leukocytes, we first

used genus-specific primers. The Mycoplasma spp. sequence was amplified from

DNA extracted from the peripheral blood of 15/28 (53.6 %) patients, whereas

specific PCR products were not detected in the 13 negative patients (46.4

%). Results were similar in female and male patients. In 32 healthy controls

without any clinical signs and symptoms, positive results were shown in 3

cases (9.4%) for Mycoplasma spp. test but not for the other species-specific

tests (0/32).

~~~~~~`

There is a lot more in this vein at www.immed.org under the autoimmune

illnesses section.