Literature DB >> 308523

Chronic permeability of the central nervous system to mononuclear cells in experimental allergic encephalomyelitis in the Lewis rat.

W Stohl, N K Gonatas.   

Abstract

In order to assess whether experimental allergic encephalomyelitis (EAE), a putative animal model for multiple sclerosis (MS), is an ongoing chronic disorder, we have studied the permeability of spinal cords of Lewis rats with EAE to 3H-uridine- or 3H-thymidine-labeled lymphoid cells obtained from thymuses of naive donors or from draining lymph nodes of donors injected with guinea pig spinal cord + complete Fruend's adjuvant (CFA), guinea pig myelin basic protein + CFA, or with CFA alone. During the acute clinical phase of EAE there is a high-level infiltration of 3H-thymidine- or 3H-uridine-labeled cells into the spinal cords. After clinical recovery from EAE up to 58 days post-inoculation, there is a low-level infiltration of 3H-thymidine-labeled cells into the spinal cords. A similar infiltration into the spinal cords by 3H-uridine-labeled cells was not detected. Donor cells from animals immunized with CFA alone showed similar levels of infiltration into the spinal cords of animals with EAE as donor cells from animals immunized with the encephalitogenic emulsion. Spinal cords from recipients immunized with CFA alone showed no increased permeability to labeled cells. Heat-killed labeled cells did not migrate into the spinal cords of animals with EAE. We conclude that a) EAE is a chronic disease and in this regard is a valid model for MS; and B) in the chronic phase of EAE, recently divided cells (3H-thymidine-labeled cells) show higher levels of migration into the target tissue than 3H-uridine-labeled cells.

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Year:  1978        PMID: 308523

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  6 in total

1.  T-cell apoptosis in inflammatory brain lesions: destruction of T cells does not depend on antigen recognition.

Authors:  J Bauer; M Bradl; W F Hickley; S Forss-Petter; H Breitschopf; C Linington; H Wekerle; H Lassmann
Journal:  Am J Pathol       Date:  1998-09       Impact factor: 4.307

2.  Localization of toxic encephalopathies near lesions of experimental allergic encephalomyelitis.

Authors:  S Levine; R Sowinski
Journal:  Am J Pathol       Date:  1982-05       Impact factor: 4.307

3.  Increased vesicular transport and decreased mitochondrial content in blood-brain barrier endothelial cells during experimental autoimmune encephalomyelitis.

Authors:  L Claudio; Y Kress; W T Norton; C F Brosnan
Journal:  Am J Pathol       Date:  1989-12       Impact factor: 4.307

4.  T cells in the lesion of experimental autoimmune encephalomyelitis. Enrichment for reactivities to myelin basic protein and to heat shock proteins.

Authors:  F Mor; I R Cohen
Journal:  J Clin Invest       Date:  1992-12       Impact factor: 14.808

5.  Experimental allergic encephalomyelitis in cynomolgus monkeys. Quantitation of T cell responses in peripheral blood.

Authors:  L Massacesi; N Joshi; D Lee-Parritz; A Rombos; N L Letvin; S L Hauser
Journal:  J Clin Invest       Date:  1992-08       Impact factor: 14.808

6.  Protection from experimental allergic encephalomyelitis conferred by a monoclonal antibody directed against a shared idiotype on rat T cell receptors specific for myelin basic protein.

Authors:  M Owhashi; E Heber-Katz
Journal:  J Exp Med       Date:  1988-12-01       Impact factor: 14.307

  6 in total

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