http://www.cnr.it/ontology/cnr/individuo/prodotto/ID268778
Temporal kinetics and cellular phenotype of TNF p55/p75 receptors in experimental allergic encephalomyelitis. (Articolo in rivista)
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- Temporal kinetics and cellular phenotype of TNF p55/p75 receptors in experimental allergic encephalomyelitis. (Articolo in rivista) (literal)
- Anno
- 1999-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/S0165-5728(98)00258-6 (literal)
- Alternative label
(a) Kahn MA, (a) Dopp JM, (a) Liva S, (b) MacKenzie Graham AJ, (a) Chang R, (a) Huang A, (a) Nazarian R, (c) Dell'Albani P, (c) Condorelli D, ( a) Voskuhl RR, (a) de Vellis J. (1999)
Temporal kinetics and cellular phenotype of TNF p55/p75 receptors in experimental allergic encephalomyelitis.
in Journal of neuroimmunology (Print)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- (a) Kahn MA, (a) Dopp JM, (a) Liva S, (b) MacKenzie Graham AJ, (a) Chang R, (a) Huang A, (a) Nazarian R, (c) Dell'Albani P, (c) Condorelli D, ( a) Voskuhl RR, (a) de Vellis J. (literal)
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- (a) Mental Retardation Research Center, Departments of Neurobiology and Psychiatry, Neuropsychiatric and Brain Research Institute, UCLA School of Medicine, Los Angeles, CA, USA; (b) Reed Neurological Research Center, Departments of Neurology, UCLA School of Medicine, Los Angeles, CA, USA; (c) Institute of Biochemistry , Faculty of Medicine , University of Catania, Sicily, Italy (literal)
- Titolo
- Temporal kinetics and cellular phenotype of TNF p55/p75 receptors in experimental allergic encephalomyelitis. (literal)
- Abstract
- TNF-alpha and LT-alpha are thought to be involved in the immunopathology of CNS demyelinating diseases. Both cytokines induce cellular effects through 55-kDa type-1 receptors (R1) and 75-kDa type-2 receptors (R2). To date, no study has specifically identified the various cell populations that express TNF receptors (TNFR) in the inflammatory and demyelinating mouse model, EAE. Phenotyping the TNFR positive cells is important in determining when and where the ligands may be acting and playing a role in disease pathology. We observed an upregulation of TNF R1 and R2 mRNA in high endothelial venules (HEVs) in the lymph node and CNS before the onset of EAE (preclinical phase). This upregulation of TNFR expression in HEVs was followed by a rapid increase in leukocytes within the CNS after the onset of clinical disease. The temporal kinetics of these data suggest that HEVs become activated early, probably through the release of pro-inflammatory cytokines originating from circulating leukocytes. An increase in TNFR on HEVs would make these cells more susceptible to TNF-induced changes, such as increasing cellular adhesion molecules, thereby further facilitating the trafficking of leukocytes into the CNS parenchyma. (literal)
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