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Contribution of tumor necrosis factor alpha to the pathogenesis of stroke

100%

Zaremba J.

Folia Morphologica

2000

tom 59

nr 3

Tumor necrosis factor alpha (TNF-alpha) is a protein of a cellular origin belonging to a group of proinflammatory cytokines. A rapid overproduction of TNF-alpha in a cerebral post-ischemic inflammatory response leads to the stimulation of adhesive molecules expression with subsequent accumulation of leukocytes in the ischemic focus, which is preceded by their adhesion and migration. The TNF-alpha proinflammatory activity results mainly in extending the area of the brain infarct, which brings about negative clinical implications. Being the final morphological effect of ischemic stroke, TNF-alpha appears also to contribute to neuronal necrosis by its involvement in the process of apoptosis as well as in the death of neurons. The present study describes and discusses mainly the contribution of TNF-alpha to the formation of ischemic focus in the brain.

Acetylcholine receptor-induced experimental myasthenia gravis: what have we learned from animal models after three decades?

67%

Baggi F., Antozzi C., Toscani C., Cordiglieri C.

Archivum Immunologiae et Therapiae Experimentalis

2012

tom 60

nr 1

Brain-derived neurotrophic factor in neuroimmunology: lessons learned from multiple sclerosis patients and experimental autoimmune encephalomyelitis models

67%

Luhder F., Gold R., Flugel A., Linker R. A.

Archivum Immunologiae et Therapiae Experimentalis

2013

tom 61

nr 2

Ograniczanie wyników

2 Archivum Immunologiae et Therapiae Experimentalis

1 Folia Morphologica

1 Antozzi C.

1 Baggi F.

1 Cordiglieri C.

1 Flugel A.

1 Gold R.

1 Linker R. A.

1 Luhder F.

1 Toscani C.

1 Zaremba J.

1 2013

1 2012

1 2000

Wyniki wyszukiwania

Contribution of tumor necrosis factor alpha to the pathogenesis of stroke

Acetylcholine receptor-induced experimental myasthenia gravis: what have we learned from animal models after three decades?

Brain-derived neurotrophic factor in neuroimmunology: lessons learned from multiple sclerosis patients and experimental autoimmune encephalomyelitis models