ABSTRACT
La esclerosis múltiple es una enfermedad inflamatoria desmielinizante que afecta el sistema nervioso central y que es considerada una de las principales causas de discapacidad en jóvenes adultos. Las causas de la esclerosis múltiple son aún desconocidas, aunque se cree que una combinación de factores genéticos y ambientales resulta en una respuesta autoinmune que promueve la degeneración neuronal/axonal. En esta revisión se analiza la asociación entre la respuesta inmune y la neurodegeneración en la esclerosis múltiple.
Multiple sclerosis is an inflammatory demyelinating disease affecting the central nervous system and considered one of the leading causes of disability in young adults. The precise cause of multiple sclerosis is unknown, although the current evidence points towards a combination of genetic and environmental factors leading to an autoimmune response that promotes neuronal degeneration. In this review, we will describe the association between the immune response and neurodegeneration in multiple sclerosis.
Subject(s)
Humans , Immunity, Cellular/immunology , Multiple Sclerosis/immunology , Nerve Degeneration/immunology , B-Lymphocytes/immunology , Inflammation/immunology , Macrophages/immunology , Myelin Sheath/immunology , Neurodegenerative Diseases/immunology , Neuroglia/immunology , T-Lymphocytes/immunologyABSTRACT
This study examined the role of the brain and peripheral connections with the target organs in the appearance of neurosecretary material within the dorsal neural sheath of the ventral ganglion of the fly S. bullata. Specifically, the accumulation of the neuropeptide FMRFamide (the neurosecretary material) was examined by immunocytochemistry. Immunoreactions were performed on: (1) a normal intact ventral ganglion, (2) an isolated ventral ganglion that was cultured in vivo, and (3) a ventral ganglion that was isolated by transection from the brain, but retained its peripheral nerve connections. The results demonstrate that (a) the neurons of the ganglia survive and exhibit FMRFamide immune reaction independent of their peripheral connections, and (b) the accumulation of neuropeptide in the dorsal neural sheath is controlled by intact peripheral nerve connections with the ganglion. It is suggested that in the absence of their peripheral connections, the axons of FMRFamide immunoreactive neurons fail to invade the neural sheath resulting in the accumulation of neurosecretary material.