“The new therapy involves programming the patient’s peripheral blood mononuclear cells, transforming them into “seed cells” to recreate pancreatic islet tissue in an artificial environment.”
I don’t see anything for the other two questions though but being patient derived would seem to fix your number 2.
Unfortunately, that doesn’t necessarily negate the requirement for immunosuppresors or some other kind of immuno protection. If it is Type 1 diabetes, the person originally became diabetic because the immune system saw certain markers on the beta cells (insulin producing cells) as a threat. So, if you recreate the beta cells, there is still a possibility that it will happen again. You are fighting your own immune system. Someone in our lab was studying encapsulation of cells to create a protective barrier around them for this very issue
If the person was Type 2, this might be less of a risk since type 2 can also be due to high insulin resistivity.
There are a lot of other factors involved, though, it’s not straightforward
1 patient, T2 since mid-30s and now 59, had kidney transplant 2017 after end-stage diabetic nephropathy and fucked glucose control since 2019. The successful cells were endoderm stem cells from him cultivated by mice they injected with his PBMCs that they then made diabetic. So not from cadavers (except mouse cadaver i guess), which is the actual new part here. Intrahepatic implant, and cells from unrelated donor failed that were embedded at the same time. His personalised mouse-donor cells worked well enough to take him off insulin 3 months later.
“The new therapy involves programming the patient’s peripheral blood mononuclear cells, transforming them into “seed cells” to recreate pancreatic islet tissue in an artificial environment.”
I don’t see anything for the other two questions though but being patient derived would seem to fix your number 2.
Unfortunately, that doesn’t necessarily negate the requirement for immunosuppresors or some other kind of immuno protection. If it is Type 1 diabetes, the person originally became diabetic because the immune system saw certain markers on the beta cells (insulin producing cells) as a threat. So, if you recreate the beta cells, there is still a possibility that it will happen again. You are fighting your own immune system. Someone in our lab was studying encapsulation of cells to create a protective barrier around them for this very issue
If the person was Type 2, this might be less of a risk since type 2 can also be due to high insulin resistivity. There are a lot of other factors involved, though, it’s not straightforward
1 patient, T2 since mid-30s and now 59, had kidney transplant 2017 after end-stage diabetic nephropathy and fucked glucose control since 2019. The successful cells were endoderm stem cells from him cultivated by mice they injected with his PBMCs that they then made diabetic. So not from cadavers (except mouse cadaver i guess), which is the actual new part here. Intrahepatic implant, and cells from unrelated donor failed that were embedded at the same time. His personalised mouse-donor cells worked well enough to take him off insulin 3 months later.
Wu, J., Li, T., Guo, M. et al. Treating a type 2 diabetic patient with impaired pancreatic islet function by personalized endoderm stem cell-derived islet tissue. Cell Discov 10, 45 (2024).
It’s good news, but you’re entirely correct that the article missed the point entirely. Thanks for the crash course in islet cell therapy!
Yeah they don’t say the type but based just on what we are discussing I would be a bet its type 2.
Hehehehehe