Assuming that was about environmental factors affecting autoimmune diabetes then there does seem to be a lot of money going into it:
Elsewhere you gave a reference to one item of the Coxsackie B research. The point I gleaned from that paper is that there is strong evidence that infections from that virus can remain inside the cells; so the virus chemical sticks around, perhaps being replicated sporadically by the cells normal reproduction machinery but it is not “expressed” in that there are no symptoms. This is like chickenpox and shingles - both variations on herpes (a symptom, like COVID) caused by the varicella virus. The virus remains embedded in cells after childhood infections then manifests in later life, perhaps when the cell reproduction machinery gets prompted to reproduce the virus DNA.
From @Chris’s Finnish reference (repeated above):
We have recently observed that CVB1 was linked to the initiation of the autoimmune process leading to type 1 diabetes in Finnish children. Viral persistency in the pancreas is currently considered as one possible mechanism.
That’s an abstract of the abstract 
, the rest of the paper (including the rest of the abstract 
is everything a good scientific paper should be. Incomprehensible.
All the same, it suggests to me that T1D responses might be sort-of like shingles or, in my case herpes opthalmicus - something that just suddenly happened to me out-of-the-blue but almost certainly reflects some previous infection. Something that doesn’t simply depend on our immune system but also depends on environmental factors which may include stuff from many, many years ago.