Multiple sclerosis and lyme disease has the IgG4 to myelin basic protein and clotting disorders. Is this a clue to how the immune system works?
heparin and myelin basic protein
https://www.ncbi.nlm.nih.gov/pubmed/29512538
MBP behave liked heparin binding lectin. Heparin strongly inhibited (MBP)
Mycobacteria's adhesion is through heparin-binding haemagglutinin adhesin (HBHA)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3103176/
spirochetes also bind to heparin
http://coolinginflammation.blogspot.com/2009/06/lyme-spirochete-binds-to-heparan-in.html
Basophils release heparin to prevent mycobacteria or spirochetes attachment to cells. (once attached these move into the cytosol of the cell where they hide)
The IgG4 in multiple sclerosis is to the myelin basic protein
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0107807
IgG4 and lyme
https://www.ncbi.nlm.nih.gov/pubmed/11987581
The autoimmune antibody IgG4 is meant to slow the immune system down during a double infection. Autoimmune cross-targeting hypothesis is that 2 infections are there and the immune system tries to ignore one infection, typically the larger one, until the smaller viral infection is killed.
Multiple sclerosis: a mycobacteria and the herpes zoster (chicken pox virus)
Normally, does the IgG2 during a mycobacteria infection actually catch some of the bacterias outside of infected cell because they bind MBP? However the body wants to figure out how to kill/ contain the viral infection before killing the cell. IgG2 usually does complement creating a surface pore on the infected cell.
Are there clotting issues with multiple sclerosis or lyme disease if heparin is around too long?
http://www.bioquicknews.com/node/1420
https://www.ncbi.nlm.nih.gov/pubmed/26821412
Article on lyme and discussing how it can resemble multiple sclerosis
https://www.nytimes.com/1995/02/15/us/personal-health-when-lyme-invades-the-brain-and-spinal-system.html
Review:
cytosol infections : TH1 : B cell: IgG2
Mitochondria/ nuclear infections Tc : B cell : IgG3
outside infections: Tfh: B cell: insulin IgG1, GH IgA, IGF-1 IgE (location hormones)
heparin and myelin basic protein
https://www.ncbi.nlm.nih.gov/pubmed/29512538
MBP behave liked heparin binding lectin. Heparin strongly inhibited (MBP)
Mycobacteria's adhesion is through heparin-binding haemagglutinin adhesin (HBHA)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3103176/
spirochetes also bind to heparin
http://coolinginflammation.blogspot.com/2009/06/lyme-spirochete-binds-to-heparan-in.html
Basophils release heparin to prevent mycobacteria or spirochetes attachment to cells. (once attached these move into the cytosol of the cell where they hide)
The IgG4 in multiple sclerosis is to the myelin basic protein
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0107807
IgG4 and lyme
https://www.ncbi.nlm.nih.gov/pubmed/11987581
The autoimmune antibody IgG4 is meant to slow the immune system down during a double infection. Autoimmune cross-targeting hypothesis is that 2 infections are there and the immune system tries to ignore one infection, typically the larger one, until the smaller viral infection is killed.
Multiple sclerosis: a mycobacteria and the herpes zoster (chicken pox virus)
Normally, does the IgG2 during a mycobacteria infection actually catch some of the bacterias outside of infected cell because they bind MBP? However the body wants to figure out how to kill/ contain the viral infection before killing the cell. IgG2 usually does complement creating a surface pore on the infected cell.
Are there clotting issues with multiple sclerosis or lyme disease if heparin is around too long?
http://www.bioquicknews.com/node/1420
https://www.ncbi.nlm.nih.gov/pubmed/26821412
Article on lyme and discussing how it can resemble multiple sclerosis
https://www.nytimes.com/1995/02/15/us/personal-health-when-lyme-invades-the-brain-and-spinal-system.html
Review:
cytosol infections : TH1 : B cell: IgG2
Mitochondria/ nuclear infections Tc : B cell : IgG3
outside infections: Tfh: B cell: insulin IgG1, GH IgA, IGF-1 IgE (location hormones)
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