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In part 2 of this Exclusive Interview, Raghu Mirmira talks with Diabetes in Control Publisher Steve Freed about the complex components that complicate the success of beta cell replacement.
Raghu G. Mirmira, PhD, MD is the director of pediatric research at Indiana University.
Transcript of this video segment:
Freed: So, you probably have a lot of information or you’re an expert when it comes to autoimmune issues. And maybe you can talk briefly about why beta cell transplantation has not really taken off and been that successful and has a lot to do with autoimmune treating that.
Mirmira: Yeah. So, again, it depends on who you talk to. The people who really advocate for beta cell transplantation certainly have an argument to make that despite the fact that sort of the gold standard, being insulin-free, isn’t achieved long-term with transplantation, that there are other benefits to transplantation such as protection from severe hypoglycemic episodes for example. And that’s true. That’s true. But part of the reason it hasn’t entirely taken off is not just because of autoimmunity, and I think that’s maybe a very small aspect of it. It’s what we call alloimmunity. You’re taking cells from somebody else and putting in somebody else. You have to use immune suppression. And those immune suppression agents also have a tendency to impact beta cells and their survival. And then there’s of course alloimmunity, that is your immune system seeing cells that are not part of you and want to reject those. And then there’s another component, of sort of an instantaneous loss of beta cells right after transplantation. It has nothing to do with immunity but what we call compliment activation, so it’s just the body’s way of just causing immediate lysis of cells, so it’s kind of complex. And really for transplantation purposes, I think we have to think about more than just autoimmunity but these other components as well.
Freed: So, what is your feeling about the regeneration of beta cells because I think recent research has shown that for type 1s that there’s still beta cell activity in some way, shape or form?
Mirmira: Yeah. And that’s actually one of the comments that I’m going to be making in my talk tomorrow. It’s that the traditional perspective that in type 1 diabetes you don’t have beta cells at all largely arose from studies in mice, right, in animals. But when we started analyzing humans we started to see that there are actual beta cells there, maybe they don’t function normally or maybe there’s not enough of them. But it certainly provides hope that maybe there’s the potential to regenerate some of these cells. And the other thing, I guess, you should ask is if we study those residual cells in somebody with type 1 diabetes, can we learn something about the cells that are most resistant to autoimmune attack and maybe those are the cells that we really need to kind of increase the amount of. And if there’s ways we cause those cells to regenerate which is possible, that might be a really more promising approach in the future.