Not only are islet cells able to be mass produced (one transplant means 150 million cells need to be created), but the challenge of the body not simply killing off these cells too through the device created at MIT really seals the deal.
Without the implatable device, this would not be as big of a breakthrough, but having both the challenge of mass producing these cells and ensuring they are able to survive after transplant without use of immunosuppressive drugs (read hardcore side effects) effectively solved makes this a real, viable solution to this problem.
Type 1 Diabetes is due to the total loss of insulin-producing pancreatic beta cells. The loss is a result of autoimmune destruction. This brings up the following questions:
1. Will the transplanted cells produce insulin in a human host?
2. Will the transplanted cells be targeted by the host's immune system and be destroyed just like the original beta cells?
3. Will the beta cells produce insulin in response to the same regulatory pathways as original system? One major problem with self-injected insulin administration is overdose.
Those are the questions I'd look to answer in the future.
I am Type 1 Diabetic. I have done some research, but am by no means an expert.
2. No. "Melton said that the device Anderson and his colleagues at Massachusetts Institute of Technology are testing has thus far protected beta cells implanted in mice from immune attack for many months. “They are still producing insulin,” Melton said."
There are two breakthroughs. The mass production AND the ability of the device to protect the cells from destruction.
3. Yes. It reacts ideally in pretty much all scenarios. When you eat, it produces insulin. When you fast, it doesn't lower you into hypoglycemia. When you're sick (like a cold) it regulates insulin as it should, as your body needs more or less as your insulin sensitivity is off.
The mice used in the protocol were SCID mice . They do not produce B or T lymphocytes (and thus no Ig either). Pretty much no adaptive immune system to speak of. These are a mainstay of murine study.
The discussion section referred to the existing technique of islet transplantation . This is sourced from cadaver tissue, and as such requires immunosuppressants. Obviously needed to counteract host v. graft, but I wouldn't be surprised if it masked the autoimmune recognition.
The discussion section alludes to several future hurdles: gene expression differences from primary cell sources, transduction response, local tissue effects (need for tissue engineering), need to produce alpha, gamma, delta, and epsilon cells (alpha and gamma may be important to precise beta function), questions regarding long-term maintenance of phenotype, ...
Nevertheless, this is very exciting! Stem cell researchers are truly hackers in every sense. The results here aren't only applicable to diabetes research, either. Patients aren't the only ones that need these cells.
I disagree. The fact they can now mass produce insulin producing islets and have a mechanism of ensuring the immune system doesn't attack them means it's very likely to be a long term cure.
The mice they have been testing have maintained their glucose at human levels for months (they generally run 60-80 points higher than humans). They've binged and fasted them, made them sick and everything and their levels have maintained.
This is definitely promising, don't be such a wet blanket before researching a little bit!
The mice were SCID mice. They have no adaptive immune system to speak of. I made another post in this thread and included some links.
This is a very incredible result though. Even if immunosuppressants are required, think of all the non-patient outcomes: easily sourced human SC-beta cells for research and high throughput study. This stuff can be grown at volume, and the techniques will only improve. The results will also inform research into other cell lines. Bottom line, this is yet another step forward for stem cell tech.
Yes, and I imagine that one possibility is to retransplant new cells as the existing ones are killed off by the immune system. Not an elegant solution to an engineer, but medicine is full of inelegant solutions.
Not to be a dick, but don't steal the limelight please.
For once, the focus is on T1 and not T1 lumped into the discussion as it usually is. Hey, I'm all for reporters putting out accurate facts(ie: knowing the differences between T1 & T2), but it's silly to act like this isn't "relevant".
T1 Diabetes is STILL extremely expensive to treat. Just because it's "only" ~10% of the total Diabetic population, doesn't equate to only ~10% of the costs incurred. T1 Diabetics account for FAR more costs(per person compared to T2) via: daily treatment, reoccurring, and emergency. Not to mention that for "most" T2 Diabetics, the disease can be easily managed via proper diet and exercise, something which CANNOT be done with T1 Diabetics.
source: someone who walks around daily with ~$8,000 worth of electronics strapped to their body everyday for the past 15 years.