Is innervation an early target in autoimmune diabetes?

In the non-obese diabetic (NOD) mouse, a spontaneous model of type 1 diabetes (T1D), recent evidence suggests that Schwann cells (Scs) and neurons surrounding insulin-producing β cells of the islets of Langerhans are destroyed before β cells. During normal perinatal development, macrophages (MΦ) are...

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Detalles Bibliográficos
Publicado: 2003
Materias:
autoantigen
chemokine
cytokine
glucose 6 phosphatase
glutamate decarboxylase
growth factor
isoenzyme
protein subunit
autoimmune disease
catalysis
cell differentiation
environmental factor
enzyme activity
genetic polymorphism
genetics
human
insulin dependent diabetes mellitus
lymphocyte
multigene family
nerve cell
nervous system
non insulin dependent diabetes mellitus
nonhuman
organogenesis
pancreas islet beta cell
protein expression
review
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14714906_v24_n11_p574_Saravia
http://hdl.handle.net/20.500.12110/paper_14714906_v24_n11_p574_Saravia
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario:In the non-obese diabetic (NOD) mouse, a spontaneous model of type 1 diabetes (T1D), recent evidence suggests that Schwann cells (Scs) and neurons surrounding insulin-producing β cells of the islets of Langerhans are destroyed before β cells. During normal perinatal development, macrophages (MΦ) are involved in phagocytosis of apoptotic neurons. Pertinently, MΦ are already present at birth in NOD pancreata. Their possible abnormal control of nerve phagocytosis, together with transient β-cell hyperactivity and lymphocyte anomalies, might conjointly participate in T1D pathogenesis.

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