Viral infections in type 1 diabetes mellitus--why the ß cells?
Nat Rev Endocrinol
; 12(5): 263-273, 2016 05.
Article
em En
| MEDLINE
| ID: mdl-27020257
ABSTRACT
Type 1 diabetes mellitus (T1DM) is caused by progressive autoimmune-mediated loss of pancreatic ß-cell mass via apoptosis. The onset of T1DM depends on environmental factors that interact with predisposing genes to induce an autoimmune assault against ß cells. Epidemiological, clinical and pathology studies in humans support viral infection--particularly by enteroviruses (for example, coxsackievirus)--as an environmental trigger for the development of T1DM. Many candidate genes for T1DM, such as MDA5, PTPN2 and TYK2, regulate antiviral responses in both ß cells and the immune system. Cellular permissiveness to viral infection is modulated by innate antiviral responses that vary among different tissues or cell types. Some data indicate that pancreatic islet α cells trigger a more efficient antiviral response to infection with diabetogenic viruses than do ß cells, and so are able to eradicate viral infections without undergoing apoptosis. This difference could account for the varying ability of islet-cell subtypes to clear viral infections and explain why chronically infected pancreatic ß cells, but not α cells, are targeted by an autoimmune response and killed during the development of T1DM. These issues and attempts to target viral infection as a preventive therapy for T1DM are discussed in the present Review.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Viroses
/
Diabetes Mellitus Tipo 1
/
Células Secretoras de Insulina
Limite:
Animals
/
Humans
Idioma:
En
Ano de publicação:
2016
Tipo de documento:
Article