Islet glia, neurons, and beta cells.
Ann N Y Acad Sci
; 1150: 32-42, 2008 Dec.
Article
en En
| MEDLINE
| ID: mdl-19120264
ABSTRACT
Type 1 diabetes (T1D) is caused by autoimmune beta cell destruction. The early events triggering T1D and the forces that keep diabetic autoimmunity pancreas specific have been unclear. Our discovery that autoimmune islet destruction is not beta-cell-exclusive but includes cytotoxic T cell targeting of peri-islet glia, evoked the possibility that T1D pathogenesis may involve neuronal elements beyond beta cell/immune interactions. Recently, we have found that sensory afferent neurons are a critical component in prediabetes initiation, promoting islet inflammation through altered glucose homeostasis and progressive beta cell stress. These factors orchestrate a catastrophic cascade culminating in insulin insufficiency mediated by an autoimmune-prone host. This neuro-immuno-endocrinological triad explains diabetic inflammation as a consequence of local neuropeptide deficiency, leading to an innovative concept of disease pathogenesis with novel therapeutic implications.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Neuroinmunomodulación
/
Neuroglía
/
Islotes Pancreáticos
/
Diabetes Mellitus Tipo 1
/
Células Secretoras de Insulina
/
Neuronas
Tipo de estudio:
Prognostic_studies
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Ann N Y Acad Sci
Año:
2008
Tipo del documento:
Article
País de afiliación:
Canadá