2025/06/25 by Deeksha Nayak, Sumit Sharma · 1 voice
Biochemistry, Genetics and Molecular Biology · Medicine · #Diabetes Management and Research #Diabetes and associated disorders #Pancreatic function and diabetes
paper · pdf · doi:10.70389/pjs.100085
openalex publication_date 2025/06/25 · openalex created_date 2025/07/01 · openalex updated_date 2026/08/01
Type 1 diabetes (T1D) is a chronic autoimmune disorder that involves autoreactive T cells, which target and destroy the insulin-producing beta cells of the pancreas. Even though there are advancements in insulin therapy and glucose monitoring, there is no particular cure for T1D, and it continues to be a potential public health problem globally. The onset of the disease is caused by genetic factors like human leukocyte antigen class II polymorphisms and environmental factors like viral infections, childhood microbiome disruption, and gut permeability. The immune response includes innate and adaptive in T1D with crucial contributors like dendritic cells, macrophages, natural killer cells, inflammatory cytokines, CD4+ and CD8+ T cells, and autoantibody-producing B cells. Chronic islet inflammation, known as insulitis, plays a significant role in disease progression. Autoantibodies are identified as the critical biomarkers for early detection of disease. Even though potential therapies like antigen-specific tolerance approaches, immune checkpoint agonists, and monoclonal antibodies like teplizumab have shown positive results, the long-term benefit remains limited. Stem-cell-based and immune cell therapies aim to restore beta cell functioning and immune tolerance but come with challenges like graft rejection and immature beta cell differentiation. Mixed strategies like stem cell therapies, immunosuppressive drugs, and gene editing should be used in treating T1D. However, a significant part of the focus should be on addressing the underlying causes of this autoimmune disorder to achieve a positive result.