amelia wrote:T cell / B cell regardless, everything is connected in some way or another to make up the immune system, which is part of the body as a whole. We all know something ain't right!
On the contrary I think the immune system is functioning very well in people with MS. It has evolved to protect us from foreign antigens and in the case of MS, the immune system confuses the foreign antigen (dietary proteins) with self tissue (myelin). The immune system in people with Type 1 diabetes also display this confusion with dietary proteins and self tissue (GAD proteins on the pancreas).
CAUSAL ENVIRONMENTAL ELEMENT: DIET
Most leading research identifies the MS equation to be: genetic susceptibility + causal environmental element – protective factor. The causal vehicle for autoimmunity is oft cited as molecular mimicry whereby the immune system launches an immune response against a foreign antigen and also self tissue. The reason for the response to both an antigen and self is the inability of the immune system to differentiate between the two.
Critical evidence of this phenomenon is found in the research by Guggenmos et al
by showing mimicry between self tissue and dietary proteins. They found that one third of their study group of PwMS had antibodies in their cerebrospinal fluid and blood that were cross reactive to each other. These antibodies were sensitized to both a protein from cow’s milk and to myelin protein; this is a very precise line of evidence supporting the mimicry process. Consider that one third of the participants had this evidence of mimicry to just one of the hundreds of proteins found in milk. Had they tested for the many more proteins in cow’s milk what would they have found?
It is worth noting that there are other food proteins with the potential to elicit an immune response against self. Celiac disease is one such beast and I would love to see Guggenmos and his cadre conduct a similar trial looking for a cross reactivity to myelin protein and gluten (or more precisely gliadin).
strongly implicates dairy as a causal element in MS and very strongly implicates dairy as a causal element in type 1 diabetes. It also demonstrates the presence of antibodies reactive to self for both diseases in a significant percentage of the study group.
Another project which corroborates the MS and Type 1 diabetes link is this study
by Winer et al in 2001 that found striking similarities between IDDM and MS. In essence, the two diseases are, by virtue of chemical markers, virtually identical. It’s only their final expression of what self tissue is attacked which differs.
A plausible explanation of the link between MS and Type 1 diabetes is that the necessary elements (genetic susceptibility + causal environmental element – protective factor) are the same for each disease save the final expression of what self tissue is assailed. Given the uniqueness of each individuals’ immune system interpretation of the perceived foreign antigen (i.e. milk protein) and how that is transcribed into an immune response, the difference in what self tissue (e.g. myelin, pancreatic GAD protein) is targeted can account for the very similar yet not exactly identical pattern of the diseases.
T cells are the body's regulators of the immune response. Increased T cell proliferation is a characteristic of autoimmune disease, in which the immune system attacks body tissues.
"However, it wasn't known whether this increased proliferation occurred early, or as a result of chronic autoimmunity," said lead researcher Brenda Banwell, MD, from the Department of Pediatric Neurology at the Hospital for Sick Children in Ontario, Canada.
The researchers studied 166 children: 63 with an autoimmune demyelinating syndrome (either multiple sclerosis or an isolated event of central nervous system autoimmunity), 43 with type I diabetes (also an autoimmune disease), 31 with a non-autoimmune neurological condition, and 30 healthy controls. They examined blood samples for T cell proliferation in response to exposure to a variety of antigens (targets), including myelin protein from nerve cells, proteins in the pancreas, and proteins in milk.
As expected, more children with central nervous system autoimmunity had T cell proliferation after exposure to myelin than control children (50 percent versus 10 percent). About a quarter of these children also showed a response to proinsulin, a T-cell target in type I diabetes. Over sixty percent also responded to a protein in milk. Ninety percent of the children with type I diabetes responded to pancreatic antigens as expected, but almost as many (79 percent) responded to myelin, and 90 percent responded to milk protein.
"Even at the onset of their disease, children with autoimmune diseases harbor T cells that will react against proteins within their tissues," Banwell said. "The responses seen against milk proteins raise the possibility that substances in food may be associated with autoimmunity."