An antibody to lymphotoxin and tumor necrosis factor prevents transfer of experimental allergic encephalomyelitis.

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An antibody to lymphotoxin and tumor necrosis factor prevents transfer of experimental allergic encephalomyelitis

Uncertainty regarding pathogenic mechanisms has been a major impediment to effective prevention and treatment for human neurologic diseases such as multiple sclerosis, tropical spastic paraparesis, and AIDS demyelinating disease. Here, we implicate lymphotoxin (LT) (tumor necrosis factor beta [TNF-beta]) and TNF-alpha in experimental allergic encephalomyelitis (EAE), a murine model of an autoim...

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nerve growth factor prevents demyelination, cell death and progression of the disease in experimental allergic encephalomyelitis

experimental allergic encephalomyelitis (eae), a demyelinating disease induced in the animals parallels multiple sclerosis in human in several aspects, provides a useful model to investigate multiple sclerosis. in this study, we have therefore used this model to study functions of nerve growth factor (ngf) in eae. ngf with considerable effects on neuron survival, proliferation and differentiati...

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A Critical Role for Lymphotoxin in Experimental Allergic Encephalomyelitis

The lymphotoxin (LT)/tumor necrosis factor (TNF) family has been implicated in the neurologic inflammatory diseases multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE). To determine the role of individual family members in EAE, C57BL/6 mice, LT-alpha-deficient (LT-alpha-/- mice), or LT-beta-deficient (LT-beta-/- mice), and their wild-type (WT) littermates were immunized wi...

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Tumor Necrosis Factor α and Lymphotoxin α Are Not Required for Induction of Acute Experimental Autoimmune Encephalomyelitis

Immunization of mice with myelin components results in experimental autoimmune encephalomyelitis (EAE), which is mediated by myelin-specific CD4(+) T cells and anti-myelin antibodies. Tumor necrosis factor alpha (TNF-alpha) and lymphotoxin alpha (LT-alpha) are thought to be involved in the events leading to inflammatory demyelination in the central nervous system. To ascertain this hypothesis 1...

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Nerve growth factor prevents demyelination, cell death and progression of the disease in experimental allergic encephalomyelitis.

Experimental allergic encephalomyelitis (EAE), a demyelinating disease induced in the animals parallels multiple sclerosis in human in several aspects, provides a useful model to investigate multiple sclerosis. In this study, we have therefore used this model to study functions of nerve growth factor (NGF) in EAE. NGF with considerable effects on neuron survival, proliferation and differentiati...

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ژورنال

عنوان ژورنال: Journal of Experimental Medicine

سال: 1990

ISSN: 0022-1007,1540-9538

DOI: 10.1084/jem.172.4.1193