Immune cells, pancreas development, regeneration and type 1 diabetes

• Published in: Trends in immunology Vol. 25; no. 5; pp. 222 - 229
• Main Authors: Homo-Delarche, Françoise, Drexhage, Hemmo A.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01-05-2004
• Subjects: Animals; Autoimmune Diseases - immunology; Autoimmune Diseases - pathology; Cytokines - physiology; Dendritic Cells - immunology; Diabetes Mellitus, Type 1 - immunology; Diabetes Mellitus, Type 1 - pathology; Disease Models, Animal; Disease Progression; Disease Susceptibility; Growth Substances - physiology; Humans; Immune System - cytology; Infant, Newborn; Inflammation; Islets of Langerhans - immunology; Islets of Langerhans - pathology; Lymphocytes - immunology; Macrophages - immunology; Mice; Mice, Inbred NOD; Mice, SCID; Models, Immunological; Morphogenesis; Pancreas - cytology; Pancreas - embryology; Pancreas - growth & development; Pancreas - immunology; Pancreas - physiology; Rats; Rats, Inbred BB; Regeneration
• ISSN: 1471-4906; 1471-4981
• DOI: 10.1016/j.it.2004.02.012

Macrophages (MΦs), dendritic cells (DCs) and lymphocytes are involved in the pathogenesis of type 1 diabetes (T1D). However, the presence of these cells is not specific for a diabetes-prone background. MΦs are also constituents of the normal fetal, neonatal and adult pancreas. We hypothesize that MΦs, DCs and lymphocytes have a role in pancreas and islet development because immune cells (particularly MΦs) are known to participate in the morphogenesis of various organs. In addition, we hypothesize that a defective function of immune cells generates an aberrant islet morphogenesis in T1D-prone individuals or animals. In the post-weaning period (a period of islet remodelling), the same defective function of immune cells might precipitate the pro-inflammatory peri-islet microenvironment that favours islet autoimmune reactivity.