alex3619
Senior Member
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- Logan, Queensland, Australia
I have said this on two other threads, but it belongs here too. I am looking at the question as to whether methylation or oxidative stress might drive the autoimmune issues. Both deplete glutathione. B cells that are glutathione deficient will not be able to make properly folded antibodies, as glutathione is needed to make sulfide bridges. I suspect that this will often inactivate the antibody, but it may also create antibodies with low or altered specificity, resulting in attacking self proteins. This would generate a very broad range of antibody targets, degrading capacity in many systems simultaneously, while also creating issues unique to individuals. It might also fit with the failure of rituximab to induce cure in many patients, as the underlying metabolic problem is not corrected. It is a testable hypothesis. Its also means that correcting oxidative and nitrosative stress might boost rituximab results. I wonder what would happen if this approach was used and included antivirals?
Cells usually have a capacity to destroy improperly folded proteins, and antibodies are proteins. However I do not know if this is right for B cells, or if they can be deranged in other ways that do this including infection. It may be that antibody production is different, or that the machinery that destroys bad proteins is failing.
What I expect to see if this hypothesis is right is large numbers of autoantibodies of different types, with different targets, but with poor binding properties.
Cells usually have a capacity to destroy improperly folded proteins, and antibodies are proteins. However I do not know if this is right for B cells, or if they can be deranged in other ways that do this including infection. It may be that antibody production is different, or that the machinery that destroys bad proteins is failing.
What I expect to see if this hypothesis is right is large numbers of autoantibodies of different types, with different targets, but with poor binding properties.