Loui

Immune system normally attacks virally infected cells because of that infected cells present mhc1. But also, virally infected cells are the self recognized cells. so it has also "don't eat me" signal on it. Although they have "don't eat me" signal how can immune system response to mhc1 and eat virally infected cells? So, if virally infected self recognized cells can be eaten by immune system, why aren't cancer cells not eaten. I know that cancer cells are self recognized also and they have don't eat me signals too. So, why immune system don't destroy them like virally infected cells? Can you advise me some articles about how immune system attacks self recognized cells? Thanks. 

4 minutes ago, iNow said:

The basic idea here is this: Should we just keep applying band-aids, or should we instead try to stop the bleeding?

Yes, we should stop bleeding but the replacement approach does not stop bleeding. Some studies are just aiming a second temporary treatment with huge budgets. Why is that happened? Because of that money? Maybe some another companies want to own this monopoly and try to find new second way to make all of the money here. Because it is a temporary way to treat the disease. After 1-2 years, patient should be treated again and again. So companies can make money continuously.

1 minute ago, iNow said:

That's a treatment, not a solution

Yes, you are right I meant it was a treatment. 

21 minutes ago, Dagl1 said:

Can you provide evidence that T1 diabetes is the result of autoimmune activity, as far as I know (but I am not very up to date in this field) we currently have no clear causal relationship, only several risk factors and some hypotheses?
If it is the case, one possibility would be to use immunosuppresive drugs in combination with this treatment, or find out if it is possible to use pluripotent stem cells of another person (potentially modified to not alert the immune system of foreign tissue). 

Dagl

Here, it says an autoimmune disease: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219937/

I wonder why scientists are trying to solve this problem by not targeting the roots of disease. We have already a solution like insulin injection, and it is a very cheap way. Our immune system can harm the new pancreatic  β celss again in 1-2 year maybe and the same processes will be repeated. So, this is not a logical approach.

Researches are studying hard to replace stem cells in type 1 diabetes. Because, pluripotent stem cells can produce functional β-like cells. But I have a question. Non-functional β cells in type 1 diabetes are the result of immune response. So, your blood consists of memory T and B lymphocytes which target your own pancreatic cells as enemy. So, even if you replace your non-functional cells, they will maintain targeting and harm your own cells. So why are the scientists trying to solve a problem in that way? If they replaced the harmed cells with functional cells, would it be a persistent treatment? Isn't it logical? 

I was searching about induced pluripotent stem cells. I read this article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6112416/ 

And it says: "While mouse cells are typically grown in a state of naïve pluripotency, equivalent to the naïve epiblast of the preimplantation blastocyst, human cells are cultured in primed pluripotency conditions. These are more similar to the postimplantation epiblast where cells become primed for differentiation."

So, hPSCs are obtained from postimplantation epiblast cells? Why don't they obtain it from preimplantation? Because preimplantation embryonic stem cells are naive pluripotent stem cells and they can differentiate into all of the germ layers. So isn't it an important reason to obtain preimplantation embryonic stem cells?