Researchers Use Protein to Reverse Multiple Sclerosis in Mice

Nobody knows what causes , the nervous system disease that affects more than 400,000 Americans, but new research sheds light on why the body is attacking itself and how to reverse it.

Researchers at the Stanford University School of Medicine have discovered how one protein could turn the tide against the degeneration found in the brains of MS patients, and actually reverse some of the worst effects of the disease.

The protein - alphaB-crystallin - is not usually found in the brain, but in the lens of the eye. It only develops in the brain in response to nerve cells that have been injured by multiple sclerosis.

Dr. Lawrence Steinman, professor of neurology and neurological sciences at Stanford, said his team showed how the protein played a protective role in mice with multiple sclerosis. "The big breakthrough in this paper is answering the question 'what is alphaB-crystallin doing,'" Steinman said in a news release.

These findings, to be published in Wednesday's online edition of Nature, also show that this protein reverses paralysis from nerve-cell injuries in mice.

“new research sheds light on why the body is attacking itself and how to reverse it.”

Please note that this article assumes facts not in evidence. In this case, the Standard Medical Myth that MS is caused by “the body ... attacking itself;” ie. an “autoimmune disease.”

Verbeek R, van Dongen H, Wawrousek EF, Amor S, van Noort JM.

Department of Biosciences, TNO Quality of Life, PO Box 2215, 2301 CE Leiden, The Netherlands.

While myelin-reactive T cells are widely believed to play a pathogenic role in multiple sclerosis (MS), no substantial differences appear to exist in T-cell responses to myelin antigens between MS patients and healthy subjects. As an example, indistinguishable peripheral T-cell responses and serum antibody levels have been found in MS patients and healthy controls to alpha B-crystallin, a dominant antigen in MS-affected brain myelin. This suggests that additional factors are relevant in allowing myelin-reactive T cells to become pathogenic. In this study, we examined whether the inflammatory state of the CNS is relevant to the pathogenicity of alpha B-crystallin-specific T cells in mice. In normal mice, T-cell responses against alpha B-crystallin are limited by robust immunological tolerance. Reactive T cells were therefore generated in alpha B-crystallin-deficient mice, and these T cells were transferred into C57BL/6 recipients. While such a transfer in itself never induced any clinical signs of experimental autoimmune encephalomyelitis (EAE) in healthy recipient mice, acute EAE could be induced in animals that had been infected 7 days before with the avirulent A7(74) strain of Semliki Forest virus (SFV). SFV infection alone did not induce clinical disease, nor did it alter the expression levels of the target antigen. Our findings indicate that at least in mice, alpha B-crystallin-specific T cells can trigger EAE but only when prior viral infection has induced an inflammatory state in the CNS that helps recruit and activate T cells.

PMID: 17267417 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17267417&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

No substantial differences appear to exist in T-cell responses to myelin antigens between MS patients and healthy subjects.

Assuming that this statement is true, then “autoimmunity” plays no or little part in the pathology of MS. But, still, the Standard Medical Myth says the opposite. Which means that all of the millions spent researching MS “autoimmunity” is meaningless.

I think that this “breakthrough” will be found to require massive amounts of fetal stem cells.

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MS Ping!