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"In a recent study ... tracked the movements of T cells that attack beta cells. These T cells find the beta cells by targeting preproinsulin, the precursor molecule to insulin.
To their surprise, the researchers discovered these T cells gather in the pancreas in nearly everyone, not just people with type 1 diabetes. Then the T cells wait. The T cells should move into the islets like hyenas, but for some reason, they can’t see their prey until some unknown event forces the islets or beta cells to “unmask” themselves. ...
Using a mouse model of type 1 diabetes, the researchers found that beta cells die off in patches that match up with where the cells are “innervated,” meaning sensitized by nerves that branch out to the pancreas.
The team found that blocking the nerve signals protected mice from beta cell death. “If the innervation is not occurring—like if you cut the nerves—then the organ remains invisible,” ...
This discovery has led ... to consider nerves as the triggers for other organ-specific autoimmune diseases. He points out that other autoimmune diseases show patterns of patchy cell death that may be linked to innervation. ...""... Many of the pre-existing “dogmas”, mostly derived from studies of animal models and sometimes limited human samples, have to be revised now. For example, we have learned that autoreactive CD8 T cells are present even in healthy individuals within the exocrine pancreas. Furthermore, their “attraction” to islets probably relies on beta-cell intrinsic events, such as the over-expression of MHC class I and resulting presentation of autoantigens such as (prepro)insulin. In addition, we are discovering other signs of beta-cell dysfunction, possibly at least in part due to stress, such as the over-expression of certain cytokines. ..."
Following two studies appear to be referenced in the above article:
New Insights Into the Role of Autoreactive CD8 T Cells and Cytokines in Human Type 1 Diabetes (open access)
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