Immune system and pancreatic beta cells

The interaction between the immune system and pancreatic beta cells is the fundamental process underlying the development of Type 1 Diabetes Mellitus (T1DM). In this autoimmune condition, the body's immune system, specifically autoreactive T-lymphocytes, targets and destroys the insulin-producing beta cells located within the islets of Langerhans (Nature Reviews Endocrinology, 2021). This destruction leads to a progressive decline in insulin secretion, eventually resulting in absolute insulin deficiency and clinical diabetes (Diabetologia, 2020). Therapeutic strategies aimed at this interaction focus on immunomodulation to preserve residual beta-cell mass and function. For instance, the anti-CD3 monoclonal antibody Teplizumab has been shown to delay the onset of clinical T1DM by interfering with T-cell mediated destruction (Herold et al., 2019; NEJM). Other approaches include B-cell depletion with Rituximab or costimulation blockade with Abatacept, although these have shown varying degrees of success in clinical trials (Diabetes Care, 2023). Monitoring the status of this interaction is typically performed through the detection of islet autoantibodies (e.g., GAD65, IA-2) and the measurement of C-peptide levels as a proxy for endogenous insulin production.

Other names

Beta-cell autoimmunityInsulitisType 1 Diabetes pathogenesisIslet autoimmunity

Immunomodulation of T-cell and B-cell activity to prevent or delay the autoimmune destruction of insulin-producing pancreatic beta cells (Herold et al., 2019; NEJM).