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
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