Diabetes type 1 II: Pathofysiologie

In type 1 diabetes, genetic and environmental factors contribute to an autoimmune response where the immune system attacks the insulin-producing beta cells in the pancreas.

These beta cells reside in clusters called the islets of Langerhans and are responsible for producing insulin, a hormone that allows glucose to enter cells for energy or storage.

As the autoimmune process unfolds, T helper 1 cells become activated and release inflammatory cytokines, such as interferon-gamma or IFN-γ, and tumor necrosis factor-alpha or TNF-α.

IFN-γ, in particular, activates macrophages and strengthens antigen presentation. These signals allow cytotoxic T cells to attack and destroy beta cells, leading to insulitis, marked by inflammation and beta cell damage in the islets of Langerhans.

Over time, ongoing inflammation progressively destroys the beta cells, drastically reducing or completely eliminating insulin production.

Without enough insulin, glucose cannot enter the body’s cells and begins to accumulate in the bloodstream.

This buildup of blood sugar leads to a condition known as hyperglycemia.