Human Nerve Growth Factor Protects Common Marmosets against Autoimmune Encephalomyelitis by Switching the Balance of T Helper Cell Type 1 and 2 Cytokines within the Central Nervous System
Autor: | Stephen L. Hauser, William C. Mobley, Stefan Fisher, Daniel P. Rosenberg, Claude P. Genain, Ilse Bartke, Jürgen W. Unger, Nathan Heald, Steven W. Cheung, Pablo Villoslada |
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Rok vydání: | 2000 |
Předmět: |
Central Nervous System
Encephalomyelitis Neurodegenerative multiple sclerosis Medical and Health Sciences Mice Myelin 0302 clinical medicine Nerve Growth Factor Immunology and Allergy Myelin Sheath 0303 health sciences Experimental autoimmune encephalomyelitis Callithrix T helper cell Immunohistochemistry Recombinant Proteins Interleukin-10 3. Good health Oligodendroglia medicine.anatomical_structure Neurological Neuroglia Encephalomyelitis Autoimmune Experimental Multiple Sclerosis 1.1 Normal biological development and functioning Immunology nonhuman primate Biology Autoimmune Disease Experimental Interferon-gamma 03 medical and health sciences Th2 Cells Underpinning research growth factors medicine Animals Humans Demyelinating Disorder Injections Intraventricular 030304 developmental biology interferon γ Multiple sclerosis Brief Definitive Report Neurosciences Th1 Cells medicine.disease Rats Brain Disorders interferon gamma Nerve growth factor nervous system Commentary interleukin 10 030217 neurology & neurosurgery Autoimmune |
Zdroj: | The Journal of experimental medicine, vol 191, iss 10 The Journal of Experimental Medicine |
ISSN: | 1540-9538 0022-1007 |
DOI: | 10.1084/jem.191.10.1799 |
Popis: | Multiple sclerosis is a demyelinating disorder of the central nervous system (CNS), in which an immune attack directed against myelin constituents causes myelin destruction and death of oligodendrocytes, the myelin-producing cells. Here, the efficacy of nerve growth factor (NGF), a growth factor for neurons and oligodendrocytes, in promoting myelin repair was evaluated using the demyelinating model of experimental allergic encephalomyelitis (EAE) in the common marmoset. Surprisingly, we found that NGF delayed the onset of clinical EAE and, pathologically, prevented the full development of EAE lesions. We demonstrate by immunocytochemistry that NGF exerts its antiinflammatory effect by downregulating the production of interferon γ by T cells infiltrating the CNS, and upregulating the production of interleukin 10 by glial cells in both inflammatory lesions of EAE and normal-appearing CNS white matter. Thus, NGF, currently under investigation in human clinical trials as a neuronal trophic factor, may be an attractive candidate for therapy of autoimmune demyelinating disorders. |
Databáze: | OpenAIRE |
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