At an immunology conference recently, I had the chance to speak with one of the leading scientists in my field. In my research, I study the role of autoantibodies in a number of weird diseases. Normally antibodies bind and neutralize bad things: bacteria, viruses, fungi. But in autoimmunity, diseases like lupus for instance, these antibodies bind to human proteins, ignoring the teleology we’ve assigned them. We think, that it’s a case of friendly fire.
But what this researcher posed to me is an important question: are the autoantibodies that I’m studying the phenomenon or an epiphenomenon? In other words, are they the cause of the disease, or a downstream byproduct of a different fundamental cause of disease.
The answer is not known right now. Which is a good thing for someone in research. From my perspective, it could be 50-50. Here’s why: we know that antibodies are sufficient in some instances to impart a phenotype but not in all. We know that for instance if someone has diptheria, if you give them just antibodies you can cure them. This demonstration won Von Behring the first Nobel Prize ever awarded.
On the other hand, the disease lupus is characterized by antibodies against double-stranded DNA. For the second half of the 20th century it was thought these antibodies caused the disease. However, if you take those antibodies and passively transfer them to a mouse, you don’t give that mouse lupus. Additionally, as early as the 1950’s it was known that some patients with lupus don’t have those antibodies. So are these antibodies epiphenomena?
Right now I’m in the process of cloning out and expressing one of these antibodies from one of these weird diseases, and within a year or two I should be able to give you something closer to an answer.