Autoimmunity occurs in MS

A

The pathogenic role of antibodies in multiple sclerosis (MS) is still controversial. We transferred to mice with experimental autoimmune encephalomyelitis (EAE), animal model of MS, IgG antibodies purified from a MS patient presenting a dramatic clinical improvement during relapse after selective IgG removal with immunoadsorption. Passive transfer of patient’s IgG exacerbated motor paralysis and increased mouse central nervous system (CNS) inflammation and demyelination. Binding of patient’s IgG was demonstrated in mouse CNS, with a diffuse staining of white matter oligodendrocytes. These data support a growing body of evidence that antibodies can play an important role in the pathobiology of MS.


As I have been saying for sometime, MSers blood contains antibodies against brain tissues and that these are not good for you. In this study they removed antibodies from an MSer and then injected them into an animal with EAE so that the antibodies could get in the brain and this made EAE worse. This clearly demonstrates that there is an autoimmune component that is ongoing in some MSers. What is does not answer is whether this is a primary or secondary problem? What is clear is that it is a problem in MS.

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MouseDoctor

14 comments

  • Well I wonder….
    There are so much things known to be harmful when having MS.
    Isn't it possible to set up a system like Dialysis for MSers?
    Filter out all the bad antibodies and Th17 cells???

    I know about Plasmapheresis, but it works different.

  • "This clearly demonstrates that there is an autoimmune component that is ongoing in some MSers"

    Wrong conclusion. This simply demonstrates that there is an autoimmune component in EAE, being there by definition.

    "…IgG antibodies purified from a MS patient presenting a dramatic clinical improvement during relapse after selective IgG removal"

    This might support your argument, but does it? Suppose there is a patient with slight brain injury after a hit of some kind. Don't you think the suppression of the immune response would prevent brain swelling and thus make the patient feel better? After all, car accident victims with severe head injuries have parts of their scull removed to allow room for swelling. In that way, immune response (swelling) might be bad for you.

    • There are innate immune response similarities in trauma and neurodegenerative disease. The goal is to control neuron cell death. Binding of patient IgG to mouse CNS is visualized on white matter oligodendrocytes. How do you discount this role of adaptive immunity?

    • Raises question of causal vs consequence for autoimmune response. Paper reinforces use of anti-B-cell therapies (Rituximab/Ocrelizumab and Alemtuzumab). Interesting that pathology of SCI and MS have similarities such as intra-lesion B-cell follicles limiting repair. Hopefully the clinical trial injecting directly into intrathecal space will be positive. Thanks for the ref.

  • Wrong conclusion. This simply demonstrates that there is an autoimmune component in EAE, being there by definition.

    Wrong way of thinking…the EAE is a tool to open the blood brain barrier to let the antibody into the brain..You don't need EAE if you inject the antibody directly into the brain.

    Oedema or swelling due to water or blood after a hit is bad news as it squishes the brain. You do not need immune response to get swelling burn yourself and you get a blister.

    You are mixing antibody responses and another different element of inflammation

  • In the US people with MS are eligible for donating blood. Seems a poor idea for the recipient if there are myelin-autoimmune cells in the blood.

    • steve sMonday, July 01, 2013 5:06:00 am

      IgM molecule that may protect OPCs and promote re-myelination.

      mmmmmmmmm………show us the evidence. The stuff published in EAE really is not that compelling as there are alternative explanations to remyelination,, the stuff in viral disease is more compelling.

      This approach has been talked about for some years ago. However and the company needs pull its socks up and start developing this. If this were a drug its paptent life would have expired long before it will get to phase IV.

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