Immune system activates after injury

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Immune system activates after injury

Postby fernando » Wed Sep 23, 2009 9:33 am

Something that we know but interesting nevertheless.

http://www.sciencedaily.com/releases/20 ... 173130.htm

"Our findings suggest that inhibiting or depleting B lymphocytes, the cells that produce antibodies, may promote healing and reduce the long-term effects of spinal cord injury," says study leader Phillip G. Popovich, professor of neuroscience and of molecular virology, immunology and medical genetics and director of the Center for Brain and Spinal Cord Repair.

"They may also help explain why the central nervous system does not repair itself efficiently and why other impairments often follow spinal cord injury."



To learn whether these antibodies could on their own damage the spinal cord, the investigators purified them from the blood of injured mice and microinjected them into one side of the spinal cord of uninjured normal mice.

Within 48 hours, the hind leg on the side of the injection site became paralyzed, and remained partially so after one week. The animals also showed loss of neurons and other damage to the spinal cord.


"This was one of the more striking, remarkable aspects of the study, the fact that the antibodies alone from an injured animal can activate an immune response that damages tissue in an uninjured animal," says Ankeny, a research scientist in molecular virology, immunology and medical genetics.

"These experiments essentially prove that the antibodies have the potential by themselves to make spinal lesions worse."
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Postby mrhodes40 » Wed Sep 23, 2009 9:44 am

Oh Thanks for that one!

THAT probably explains why Campath is helpful as it is a reboot of everything including b cells.

It has been known for some time that a good part of spinal cord injury is related to the immune response and not the trauma and they have been trying immune suppression after the fact to ameliorate it. Obviously spinal cord injury is not an autoimmune anything............ :lol:

So if we extrapolate and say that CCSVI damage is similar to trauma in that nerve tissue is damaged, then it is reasonable to say that in CCSVI an overactive immune response is part of the problem. In fact it is known that in venous ulcers the body's own immune response causes increased damage.

I have said that it may be true that the final best treatment for CCSVI includes some form of suppression either just before or after the surgery. Hopefully such a thing would be temporary....

us early folks get the 'best guess' therapy version :wink:
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Postby SammyJo » Wed Sep 23, 2009 2:26 pm

I just said I was going to be quiet til I'm smarter... but here I go again.
Immune supression... or regulation. This article is from 2007, I don't know if there has been any progress down the kinder gentler path of regulation. There should be something, because it is being looked at for many tissue injuries that stimulate autoimmunity - myocardial infarction, spinal injury, MS...well, at least there's LDN for immune system calm.

T effectors outfox T regulators in autoimmunity
Findings from a mouse model of multiple sclerosis suggest that regulatory T cells alone cannot outduel pathogenic T
cells in the central nervous system. The observations may have implications for experimental approaches designed to
dampen autoimmune diseases by infusion of regulatory T cells.
http://www.neuroimmunol.org/papers/nm0407-411.pdf
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Postby fernando » Thu Sep 24, 2009 3:05 pm

Thanks to you Marie for your ever insightful comments.

Fernando
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Postby cheerleader » Fri Sep 25, 2009 5:20 pm

Here's an interesting study showing how Copaxone modulates t-cells after ischemic stroke in mice...

perhaps we're coming to an understanding as to the mechanism of these medications in the CCSVI paradigm?

Abstract

The damage in ischemic stroke is caused by two events: (i) the ischemic phenomenon by itself; (ii) the self-destructive mechanisms developed as a consequence of ischemia. The inflammatory response is one of these destructive phenomena that accompanies and exacerbates the developing injury. Since it has been suggested that immune cells participate in neuroprotective and restorative processes, modulation rather than elimination of this inflammatory response could be a strategy to improve the neurological outcome. The immune modulator copolymer-1 (Cop-1), a synthetic basic random copolymer of amino acids, is a potent inducer of Th2 regulatory cells which, aside from exerting modulatory actions, is capable of releasing neurotrophic factors. There is evidence that Cop-1-specific T cells exert neuroprotective and even restorative effects in diverse neurodegenerative diseases. In order to test the ability of Cop-1 to prevent ischemic injury in a model of transient middle cerebral artery (MCA) occlusion, two groups of rats were treated either with Cop-1 or with saline solution (SS). Seven days after occlusion, Cop-1 treated rats presented a significant improvement in neurological function compared to SS-treated animals (1.2 ± 0.4 and 2.8 ± 0.5 mean ± S.D., respectively; p = 0.008). Histological findings showed that the percentage of infarct volume was smaller in Cop-1 treated rats (4.8 ± 1.5), in comparison with those receiving SS (32.2 ± 8.6; p = 0.004). Cop-1 constitutes a promising therapy for stroke; thereby, the enforcement of further experimental investigation is encouraged in order to be able to formulate the best strategy.


link

Jeff has stayed on his copaxone thruout the stenting procedure...it was his call, and I think his instincts were good....
cheer
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dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby DIM » Sat Sep 26, 2009 12:24 am

Which has fewer side effects than every other known MS drug (except supplements, LDN etc but those aren't accepted drugs) Cheer!
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Postby mrhodes40 » Sat Sep 26, 2009 10:09 am

I take cop too, it makes some pretty sore lumps but in 12 or so years of taking I have never had anything remotely bad in terms of reaction. It also controls me RA really well.........

sadly the stuff is off patent and they will not be testing it for RA or other inflammatory diseases.
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Postby DIM » Sat Sep 26, 2009 11:04 am

mrhodes40 wrote:I take cop too, it makes some pretty sore lumps but in 12 or so years of taking I have never had anything remotely bad in terms of reaction. It also controls me RA really well.........

sadly the stuff is off patent and they will not be testing it for RA or other inflammatory diseases.

Quite interesting you suffer from RA and MS usually those diseases don't go together, by the way what are your uric acid levels?
MSers have them low while RA sufferers very high!
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Postby sou » Sat Sep 26, 2009 11:24 am

Hi.

I think that high levels of UA are not associated with RA but a completely different type of arthritis.

sou
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Postby whyRwehere » Sat Sep 26, 2009 11:27 am

I think my husband is allergic to copaxone...he had that chest reaction too often, followed by chills and hives, and over time weight loss.
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Postby mrhodes40 » Sat Sep 26, 2009 4:18 pm

Yes sou is correct gout is high UA...i have rheumatoid

BUT RA is not common with MS that is true too. Luckily my RA is fairly mild, I am not sure I could take bad cases of both. My MS is pretty progressed.

I am very special. :roll:
I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
http://www.thisisms.com/ftopic-7318-0.html This is my regimen thread
http://www.ccsvibook.com Read my book published by McFarland Health topics
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