Immune Responses in Type 1 Diabetes
A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".
Deadline for manuscript submissions: closed (28 February 2026) | Viewed by 17850
Special Issue Editors
Interests: human type 1 diabetes; autoimmunity; T cell immunity; target tissue
Special Issue Information
Dear Colleagues,
Type 1 diabetes (T1D) represents an archetypical polygenic autoimmune disease that renders patients insulin-dependent through the depletion of functional pancreatic beta cells via a combination of direct killing, apoptosis, and cellular dysfunction. The management of the disease requires a precisely administered insulin regimen to avoid ketoacidosis due to acute, severe hyperglycemia and long-term complications due to the accumulated effects of glucose excursions while avoiding hypoglycemia. The risk for the development of T1D can be predicted through the occurrence of biochemically defined islet autoantibodies. Furthermore, the genetic risk for the disease is dominated by the HLA class II locus, along with HLA class I and a broad number of immune response-related genes with more modest effect sizes. Early histological studies and more recent and elegant studies of human pancreatic tissue from organ donors have consistently revealed the HLA class I expression and document infiltration of the islets by multiple types of immune cells, including CD8+ and CD4+ T cells, gamma delta T cells, myeloid cells, NK cells, B cells, and CD11c+ antigen presenting cells. The role that these varied immune cell populations play in the disease process remains an important area of active investigation. In spite of the recent efforts, only limited information exists regarding the antigen and epitope specificity of islet-infiltrating T cells, but the existing literature confirms the presence of both autoreactive and bystander T cells. Accumulating studies also support the existence of an ongoing dialog between immune cells and pancreatic beta cells, which may include both disease-promoting and disease-restraining effects. Exploring this complex landscape offers the opportunity to unravel underlying causes of disease, sources of heterogeneity, and avenues for effective intervention.
Therefore, the goal of this Special Issue, entitled “Immune Responses in Type 1 Diabetes", is to provide a broad overview of the contribution of various immune cell subsets to disease development and etiology, including knowledge gained through the study of human subjects and animal models of the disease. This Special Issue aims to provide insights about the dialog between immune cells and pancreatic islets, including mechanisms that promote or restrain diabetes progression. Original research using conventional (e.g., immunohistochemistry, cell culture, flow cytometry) and more advanced methods of tissue and cellular characterization (e.g., scRNA-Seq and scATAC-Seq) are invited, as are well-balanced review articles. We welcome your contributions to this important Special Issue.
Dr. Eddie A. James
Dr. Sally C. Kent
Guest Editors
Manuscript Submission Information
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Keywords
- type 1 diabetes
- insulitis
- immune response
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