@Abolitionist,
What the wiki article is probably refererring to are translocation events that happen whenever you have DNA recombination or rearrangement. While the word "mutation" can refer very broadly to things that alter DNA, the diversity of antibodies can be accounted for with VDJ rearrangements alone.
Abolitionist wrote:I think that in some ways, we may be better off changing our biology so that we are less complex down the road, but no specific examples to be used for the present come to mind right now
I disagree with the idea of changing our biology except in extremely small, targeted cases. I think our complexity 1) prevents us from being fully understood such that we CAN manipulate our biology except in clear cut cases of disease, and 2) our complexity evolved over the entire biological history of our lineage, and while we have genetic diseases and junk DNA, even a small statistical effect on survival or adaptability can have enormous population effects. Organisms that are specialized and who lose ancestral "general" features become what is called 'terminally differentiated', which means they cannot adapt to change. That's a recipe for extinction.
Quote:makes me wonder if there is a potential way to remove specific antibodies or even turn the immune system against antibodies which cause autoimmune disorders
This is not all about antibodies. Most autoimmune diseases require the input of T cells. Antibodies come from B cells. You need to do some reading about the T cell receptor (which has comparable diversity to antibodies), and in particular you need to read about the HLA molecules (human leukocyte antigen), otherwise known as MHC (the major histocompatibility complex).
You also need to read about the maturation process of B cells in the bone marrow and T cells in the thymus, by which lymphocyte clones that produce auto-reactive antibodies and T cell receptors become removed. In other words, we have an endogenous mechanism during fetal development and early childhood to eliminate autoimmunity.
There isn't really a way to eliminate a
specific kind of autoantibody, because it's a moot point if you're not eliminating the clone of B cells that's making it. There are things like IVIG (intravenous immune globulin), plasmapheresis, and immunosuppressive drugs that can nonspecifically suppress the activity and level of autoantibodies in various antibody-mediated autoimmune diseases. These therapies all come at a price, but we don't have a way of mimicking the body's innate ability to select out autoactive lymphocytes.
Quote:to buy time, we might be able to give the autoimmune disorders 'something to chew on' besides our needed parts by injecting antigens that would bind to those antibodies before they can do damage
That doesn't tend to work very well, and in fact could make things a lot worse. Give a bunch of antigen and you get antigen-antibody complexes that will activate the complement pathway, deposit in the kidneys, deposit in blood vessels, and cause all kinds of autoimmune havoc.
And in fact the autoantibodies in lupus, Sjogren's syndrome, rheumatoid arthritis are not only attacking native tissue -- they're binding to circulating endogenous molecules that already exist in great abundance in the body, and they specifically cause disease through the formation of antigen-antibody complexes. So just giving
more of their target antigen won't change anything.
The latest and greatest therapies for autoimmune diseases are biological, i.e. they target specific cytokines (molecules by which inflammatory cells talk to each other). The most famous examples are inhibitors of TNF-alpha, like etanercept (Enbrel), infliximab (Remicade), and adalimumab (Humira). These are extremely useful for Crohn's disease and rheumatoid arthritis. Of course the T-cell mediated granulomatous response that is pathologic in Crohn's disease is the same kind of immune response that protects you against tuberculosis and some other infections -- so sure enough I've seen some wild and terrible infections in people on these drugs.