What exactly is the reasoning behind treating some autoimmune disorders (ITP, MS, myasthenia gravis, etc) with IV immunoglobulins? I can understand how antibodies might be of use in treating immune deficient patients, but what exactly are they doing in patients whose own antibodies are overreacting to self antigens?
All I can come up with is that maybe it’s a question of sheer numbers - with so many different antibodies in the blood, there’s less chance of the auto-antibodies finding and binding their targets. Considering the specificity of antibodies, though, I don’t know how likely that is.
If any medical Dopers can explain it to me, or even just point me towards a helpful article, I’d be much obliged!
I’m a little confused by your question because, IIRC, antibody and immunoglobulin are interchangable terms.Wikipedia seems to agree with me, anyway.
If they are the same thing, then likely what is going on is that the antibodies given by the doctor attach to the antibodies the body made against it’s own cells. By binding up the bad antibodies this way, the antibodies the doctor gave would prevent the cells from being tagged for destruction by the bad antibodies.
Just my Wild-ass second year vet student guess. Any and all human medical professionals correct me.
Yes, I know they’re the same thing. Lookit my username, fercryingoutloud!
Thanks for the link, groman. Tying up the macrophage receptors makes sense, but don’t the antibodies have to be bound to antigen before being recognized at the receptor? Same for complement, no? So what in the world are the antibodies binding?
Basically, the links I’ve been finding tell me that we know it works because we’ve seen it work, but we’re not really sure why it works. I hate when there’s no why!
I think that summed it up pretty well. I will just want to add that sometimes when the IVIG isn’t acting effectively another method of combating some of these disorders is the procedure Plasma Pheresis Exchange. Where instead of eliminating the antibodies the general premise becomes diluting them out. The ill patient is put onto a pheresis instrument and has her own plasma removed, while at the same time being transfused with a large amount of donor plasma. This procedure is usually performed a number of times depending on the strength of the antibodies.
Plasma pheresis exchange is also therapy for many other illnesses, like some forms of cancer and severe cases of malaria.
So my hypothesis about the exogenous antibody being targeted for the harmful, endogenous antibody is one of the going theories. But now I’m confused about why they think activation of the complement pathways would decrease signs of cell lysis. I mean, to oversimplify, isn’t cell lysis what the complement system does? And if cell lysis is generally the root of autoimmune diseases, wouldn’t activating more complement be bad? What am I missing?
It’s not fair for the hamsters to post my posts when I’ve only got them half way thought out.
So my hypothesis about the exogenous antibody being targeted for the harmful, endogenous antibody is one of the going theories. But now I’m confused about why they think activation of the complement pathways would decrease signs of cell lysis. I mean, to oversimplify, isn’t cell lysis what the complement system does? And if cell lysis is generally the root of autoimmune diseases, wouldn’t activating more complement be bad? What am I missing?
