Also it's AFAIK the only explanation we have for MS lesions exclusively towards veins. If the immune system would simply decide to act up at some point we'd expect the lesions to be more scattered as in EAE, wouldn't we?
I don't know, but, no matter what the cause of MS, no one questions that immune cells are migrating from blood vessels into the brain tissue. So, it wouldn't be too much to assume that most of the damage will take place near the site of the migration, i.e. the blood vessels.
However as you say, ballooning comes currently has the practical problem that stenoses re-ocurr and patients relapse relatively quickly after that (to be precise we don't know how many of the relapse-free patients of Zamboni have had re-stenoses). A possible explanation for this is that the areas of lesions are still frail, and if the stenosis suddenly kicks in again this leads to renewed disruption. Additionally it could be that the immune system has continuously eroded the areas of endothelium disruption/microbleeds/lesions, making it harder for these disruptions to heal.
I guess that's one possible explanation. But when people receive IV steroids to quicken the recovery from an attack, after the attack resolves, they don't immediately have another one.
Quick question: are there reliable data on after how many months/years the T&B cell populations fully recover post Campath infusion?
I'm not sure. Maybe someone here who had received Campath could answer. I know as part of the trial, monthly blood draws are done to check platelet counts, but I'm not sure about WBC counts.