The basic definition of type 1 development is such – the loss of insulin-producing pancreatic beta-cells, with all its implications.
However, as soon as there is talk about the underlying processes, we reach a zone of opinions and speculations. The majority of those refer to a complex interplay of the immune system, environmental factors and genetic susceptibility. A common agreement, though, is that the nature of the death of beta-cells is exceedingly complex.
One of the latest perspectives on the cause of type 1, involves the nature of pancreatic beta-cells and their demise. It relates to a mix of ‘homicide’ and ‘suicide’ of the cells – immune responsiveness (homicide) and the specific beta-cells fragility (suicide).
So, while the idea of beta-cells homicide is fairly common knowledge, the suicide one is not as common. The idea is that autoimmune response cannot by itself perpetuate the destruction of enough beta-cells. On the other hand physiologic changes of the beta-cells in response to the autoimmune actions (or unknown environmental factors) may be critical to perpetuating the beta-cell autoimmunity. Studies have suggested that some islets remain with intact beta-cells, even in patients with long-term type 1. While the surviving beta-cells are not normal and functioning, this bring more light to the picture and explains the (usually) very slow progression of beta-cell loss.
Studies also confirm that beta-cells survive in many patients with established type 1, but at the same time are unable to produce enough insulin to overcome the hyperglycemia. It is thought that the hyperglycemia is one of the perpetuating factors of the beta-cell death, causing the cells to reach a dysfunctional threshold. This is confirmed by recent efforts of successful interruption, by means of bone marrow transplant and immunosuppression, of the beta-cell destruction, and achieving at least temporary insulin independence.
The honeymoon, experienced after initial treatment with insulin, may actually reflect reversal of the beta-cell suicide effect. As is the case though, this alone is not sufficient to fully reverse autoimmunity.
However, better understanding on the processes of immune-mediated and cellular death, can and has improved immune therapies, preventing and reversing beta-cell death.