2000
DOI: 10.1016/s0165-5728(99)00242-8
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Analysis of experimental autoimmune encephalomyelitis induced in F344 rats by pertussis toxin administration

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Cited by 20 publications
(12 citation statements)
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“…This is similar to other autoimmune disease models, such as experimental autoimmune encephalomyelitis (EAE). Administration of PT concurrently with uveitogenic immunization permits expression of disease in resistant strains, and enhances it in susceptible strains (15, 24, 25). The mechanism has for a long time been thought to involve the opening of the blood–organ barrier by PT (26, 27); however, recently we showed that a dominant effect of PT in EAU is to enhance the Th1 response and the Th17 response, both pathogenic in EAU (15, 24, 28).…”
Section: Introductionmentioning
confidence: 99%
“…This is similar to other autoimmune disease models, such as experimental autoimmune encephalomyelitis (EAE). Administration of PT concurrently with uveitogenic immunization permits expression of disease in resistant strains, and enhances it in susceptible strains (15, 24, 25). The mechanism has for a long time been thought to involve the opening of the blood–organ barrier by PT (26, 27); however, recently we showed that a dominant effect of PT in EAU is to enhance the Th1 response and the Th17 response, both pathogenic in EAU (15, 24, 28).…”
Section: Introductionmentioning
confidence: 99%
“…The CDC reported in 2001 that neurological complications such as encephalopathies occur in 0.1% of all reported pertussis cases probably as a result of hypoxia from coughing or possibly from toxin activities (CDC, 2002). Several studies showed that the exotoxin pertussis toxin (PT) apparently contributes to the disruption of cerebral barriers (Geier and Geier, 2004;Grant et al, 1998;Amiel, 1976;Arimoto et al, 2000). PT has been shown to facilitate the onset of experimental autoimmune encephalomyelitis (EAE) in mice, a surrogate animal model to study the pathological mechanisms of the human demyelinating disease multiple sclerosis (Arimoto et al, 2000;Lehmann and Ben-Nun, 1992;Linthicum et al, 1982).…”
Section: Introductionmentioning
confidence: 99%
“…Several studies showed that the exotoxin pertussis toxin (PT) apparently contributes to the disruption of cerebral barriers (Geier and Geier, 2004;Grant et al, 1998;Amiel, 1976;Arimoto et al, 2000). PT has been shown to facilitate the onset of experimental autoimmune encephalomyelitis (EAE) in mice, a surrogate animal model to study the pathological mechanisms of the human demyelinating disease multiple sclerosis (Arimoto et al, 2000;Lehmann and Ben-Nun, 1992;Linthicum et al, 1982). In previous studies in our laboratory, we demonstrated a PT-induced increase in permeabilization of cerebral endothelial barriers in tissue culture models that in turn increases the migration of human monocytes across the endothelial barrier (Kügler et al, 2007).…”
Section: Introductionmentioning
confidence: 99%
“…This assumption may however not be conclusive as recent data suggest that PTx increases expression of cerebrovascular adhesion molecules [15], [16], proposing an alternative mechanism by which PTx may facilitate leukocyte migration into the CNS. PTx further promotes maturation and functional capacity of antigen presenting cells (APC) [17], increases production and release of pro-inflammatory cytokines such as IL-12 [18] and decreases secretion of anti-inflammatory IL-10 [19]. When used as an adjuvant for EAE induction, PTx reduces number and function of Treg [20], [21], while promoting development of encephalitogenic Th17 cells[22], [23].…”
Section: Introductionmentioning
confidence: 99%