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<blockquote data-quote="Shemeska" data-source="post: 2196781" data-attributes="member: 11697"><p>Color me underwhelmed.</p><p></p><p>She's still going to be on immune suppressants for the rest of her life. A true cure for diabetes is going to require 2 things:</p><p></p><p>1) Suppression of the abberant T cell mediated autoimmune attack on mature islet cells, or the destruction of those cells specific to the response.</p><p></p><p>2) Replacement of the islets.</p><p></p><p>Most research that gets to the press or is lauded by the major diabetes groups are a false hope since they don't do a thing to solve the 1st issue above. Anti rejection drugs have problems in and of themselves, and the long term survival rate for transplanted islets isn't all that good.</p><p></p><p>There has been some work in the past 4 years or so trying to solve the immune issue entirely. Experiments, first published in the journal Science, by Faustman et al have demonstrated that TNF alpha at certain concentrations causes active T cells in mice, aka those involved in the destruction of islet cells constantly, to undergo apoptosis. Not only that, but they also found that the mice regained normal blood sugar levels shortly after that. Further investigation found that the islets were regenerating via precursor cells from the spleen, and that this was constant even in late stage diabetics in which there were no active islet cells at the start of treatment with TNFa.</p><p></p><p>The mice they've used have their diabetes caused by the exact same T cell autoimmune response that is present in humans, making them a very effective model for the disease. Also, there's now published evidence to suggest that human islets also are derived from spleenocyte precursors. End result being if you shut off the immune response in type one diabetics you could end disease.</p><p></p><p>Other experiments have worked in mice using spleenocytes from other mice to ameliorate the immune response in the diabetic animals.</p><p></p><p>Faustman has been approved for stage 1 clinical trials in humans of, last I checked, one off patent drug that induces TNFa production by the body. I've got my fingers crossed.</p><p></p><p></p><p>Other recent research has involved a paper to be published in the journal Gastroenterology. Researchers working to create beta islet cells from a line of adult stem cells applied the same growth factors to unsorted leukocytes (human). They injected the cells into diabetic mice and found that the animals blood sugar levels normalized for a period of time before their immune systems rejected the human cells. Apparently the white cells had been prompted into producing insulin in response to high blood sugar levels. This is interesting since I wouldn't have suspected it, and the induced cells might not be recognized by the T cells that otherwise destroy islet cells. I'd also worry about how it might affect certain type of white cells (ie immature B cells, memory cells, plasma cells) over a long period of time.</p></blockquote><p></p>
[QUOTE="Shemeska, post: 2196781, member: 11697"] Color me underwhelmed. She's still going to be on immune suppressants for the rest of her life. A true cure for diabetes is going to require 2 things: 1) Suppression of the abberant T cell mediated autoimmune attack on mature islet cells, or the destruction of those cells specific to the response. 2) Replacement of the islets. Most research that gets to the press or is lauded by the major diabetes groups are a false hope since they don't do a thing to solve the 1st issue above. Anti rejection drugs have problems in and of themselves, and the long term survival rate for transplanted islets isn't all that good. There has been some work in the past 4 years or so trying to solve the immune issue entirely. Experiments, first published in the journal Science, by Faustman et al have demonstrated that TNF alpha at certain concentrations causes active T cells in mice, aka those involved in the destruction of islet cells constantly, to undergo apoptosis. Not only that, but they also found that the mice regained normal blood sugar levels shortly after that. Further investigation found that the islets were regenerating via precursor cells from the spleen, and that this was constant even in late stage diabetics in which there were no active islet cells at the start of treatment with TNFa. The mice they've used have their diabetes caused by the exact same T cell autoimmune response that is present in humans, making them a very effective model for the disease. Also, there's now published evidence to suggest that human islets also are derived from spleenocyte precursors. End result being if you shut off the immune response in type one diabetics you could end disease. Other experiments have worked in mice using spleenocytes from other mice to ameliorate the immune response in the diabetic animals. Faustman has been approved for stage 1 clinical trials in humans of, last I checked, one off patent drug that induces TNFa production by the body. I've got my fingers crossed. Other recent research has involved a paper to be published in the journal Gastroenterology. Researchers working to create beta islet cells from a line of adult stem cells applied the same growth factors to unsorted leukocytes (human). They injected the cells into diabetic mice and found that the animals blood sugar levels normalized for a period of time before their immune systems rejected the human cells. Apparently the white cells had been prompted into producing insulin in response to high blood sugar levels. This is interesting since I wouldn't have suspected it, and the induced cells might not be recognized by the T cells that otherwise destroy islet cells. I'd also worry about how it might affect certain type of white cells (ie immature B cells, memory cells, plasma cells) over a long period of time. [/QUOTE]
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