Sorry to bump up an old thread. Some of my post is about debates that are old hat here, but what can I do, I have 2 cents and want to toss em in.
Raven, I think youre quite right that the Prineas apoptotic lesion could quite conceivably be caused by antibody in principle. Therefore the Prineas finding does not disprove an autoimmune cause of the apoptotic lesion. Prineas and Barnett acknowledged this point in print in a reply to a letter-writer who emphasized it.
You point out that Prineas and Barnett went searching for the apoptotic lesions in specific, and that they arent common. But, they didnt focus on this lesion type due to some unjustified fixation on it. Rather, they focused on it with the thought that most or all lesions might start out as apoptotic lesions, but rapidly lose their identifiability as such. Whether or not that is true is very difficult to directly determine, since opportunities to cut up and examine a brand-new lesion are exceedingly rare. But its a plausible proposition.
I dont think its vain for people who arent research professionals to dissent from the professionals' consensus - because when I look at what the pros say, I see no consensus. And theres reason for that. As far as I can tell no one has found a specific autoreactivity that is unique to MS. MS has some hefty HLA type associations, but so does leprosy. MS responds to immune depressants; so too do some infectious diseases. I've been just astonished by the causal statements by medical professionals, etc, that MS "is" an autoimmune disease. How sloppy that is! It needs to stop. IMO you cant blame people for being rankled by this, when they find out just how uncertain things really are.
I dont have MS, but I study all diseases of immune activation. I had severe CFS and am 95% well, 1 yr into antimicrobial treatment.