Posted: Sun Jul 01, 2007 1:48 am
Sharon,
Lyndacarol,
Dr Meggs seems to have a strong opinion on the way the immune system communicates with the nervous system. Obviously I'm not able to evaluate the quality of his theories, but I know that there are other ways to interpret the reason for immune system activity, too.
Have you heard about Polly Matzinger and her "danger model"? If she's right, there wouldn't be "autoimmune reactions" at all. Quote:
"In a 1994 article entitled "Tolerance, Danger and the Extended Family", Matzinger went several steps further by laying out the idea that antigen-presenting cells respond to "danger signals" - most notably from cells undergoing injury, or stress or "bad cell death" (as opposed to apoptosis, controlled cell death). The alarm signals released by these cells let the immune system know that there is a problem requiring an immune response. She argued that T-cells and the immune response they orchestrate does not occur because of a neonatal definition of "self", as in the previous model, nor because of ancient definitions of pathogens, as in Janeway's argument, but on a dynamic and constantly-updated response to danger as defined by cellular damage."
So, if Matzinger is right, the immune response would be a reaction to abnormal cell death, not the primary reason for nerve damage.
Be well,
-finn
Interesting study, thanks for sharing it! I agree with you, there is the possibility that immune system activity in MS is not an "autoimmune reaction" at all.Shayk wrote:I accidentally happened across an abstract that seems to suggest that autoreactive T or B cells might in fact be protective. It seems to be consistent with the idea that inflammation may be neuroprotective.
Well, this is a consensus autoimmune board now, and I try not to corrupt the spirit by posting more here :-) But if I find something really interesting, I promise I'll make an exception and share it.Shayk wrote:I'm definitely not in the auto-immune camp. ;-) And, if you come across more info from Tsunoda and Fujinami I do hope you'll post it.
So far I have come across two things that may be able to increase BDNF: exercise and some antidepressants. Do you happen to have information on other substances that might be able to do it?Shayk wrote:(btw-- My interest is really in BDNF since some researchers seem to be hard at work trying to figure out how to deliver it to our brains and spinal cords for neuroprotection and to prevent neurodegeneration.)
Lyndacarol,
Dr Meggs seems to have a strong opinion on the way the immune system communicates with the nervous system. Obviously I'm not able to evaluate the quality of his theories, but I know that there are other ways to interpret the reason for immune system activity, too.
Have you heard about Polly Matzinger and her "danger model"? If she's right, there wouldn't be "autoimmune reactions" at all. Quote:
"In a 1994 article entitled "Tolerance, Danger and the Extended Family", Matzinger went several steps further by laying out the idea that antigen-presenting cells respond to "danger signals" - most notably from cells undergoing injury, or stress or "bad cell death" (as opposed to apoptosis, controlled cell death). The alarm signals released by these cells let the immune system know that there is a problem requiring an immune response. She argued that T-cells and the immune response they orchestrate does not occur because of a neonatal definition of "self", as in the previous model, nor because of ancient definitions of pathogens, as in Janeway's argument, but on a dynamic and constantly-updated response to danger as defined by cellular damage."
So, if Matzinger is right, the immune response would be a reaction to abnormal cell death, not the primary reason for nerve damage.
Be well,
-finn