Advances in the cellular immunological pathogenesis of type 1 diabetes

• Published in: Journal of cellular and molecular medicine Vol. 18; no. 5; pp. 749 - 758
• Main Authors: Li, Min, Song, Lu‐Jun, Qin, Xin‐Yu
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01.05.2014; BlackWell Publishing Ltd
• Subjects: Antigen-Presenting Cells - immunology; Antigens; Autoantigens - metabolism; autoimmune disease; Autoimmune diseases; Beta cells; CD4 antigen; CD8 antigen; Cell-mediated immunity; Cytokines; Dendritic cells; Diabetes; Diabetes mellitus; Diabetes mellitus (insulin dependent); Diabetes Mellitus, Type 1 - etiology; Diabetes Mellitus, Type 1 - immunology; Diabetes Mellitus, Type 1 - pathology; Disease prevention; Humans; Immune response; Immunity, Innate; immunological mechanism; Immunology; Immunoregulation; Immunosuppression; Insulin; islet cells; Killer Cells, Natural - immunology; Kinases; Lymphocytes; Lymphocytes T; Natural killer cells; Pancreas; Pathogenesis; Proteins; Review; T lymphocyte; Toxicity; type 1 diabetes; type 1 diabetes; islet cells; T lymphocyte; immunological mechanism; autoimmune disease
• ISSN: 1582-1838; 1582-4934
• DOI: 10.1111/jcmm.12270

Type 1 diabetes is an autoimmune disease caused by the immune‐mediated destruction of insulin‐producing pancreatic β cells. In recent years, the incidence of type 1 diabetes continues to increase. It is supposed that genetic, environmental and immune factors participate in the damage of pancreatic β cells. Both the immune regulation and the immune response are involved in the pathogenesis of type 1 diabetes, in which cellular immunity plays a significant role. For the infiltration of CD4+ and CD8+ T lymphocyte, B lymphocytes, natural killer cells, dendritic cells and other immune cells take part in the damage of pancreatic β cells, which ultimately lead to type 1 diabetes. This review outlines the cellular immunological mechanism of type 1 diabetes, with a particular emphasis to T lymphocyte and natural killer cells, and provides the effective immune therapy in T1D, which is approached at three stages. However, future studies will be directed at searching for an effective, safe and long‐lasting strategy to enhance the regulation of a diabetogenic immune system with limited toxicity and without global immunosuppression.