Absence of the memory response to encephalitogen following intergender adoptively transferred experimental autoimmune encephalomyelitis

Abstract Animals that have recovered from adoptively transferred EAE develop clinical disease signs 2–3 days earlier than controls when challenged with encephalitogen. This may be due to the reactivation of donor-derived memory cells or stimulation of recipient-derived memory cells primed during the...

Full description

Saved in:
Bibliographic Details
Published in:Journal of neuroimmunology 2015-01, Vol.278, p.194-199
Main Authors: Archie Bouwer, H.G, Gregory, Cynthia R, Wegmann, Keith W, Hinrichs, David J
Format: Article
Language:English
Subjects:
Adoptive transfer
Adoptive Transfer - methods
Allergy and Immunology
Animals
Disease Models, Animal
Encephalomyelitis, Autoimmune, Experimental - immunology
Encephalomyelitis, Autoimmune, Experimental - therapy
Experimental autoimmune encephalomyelitis
Female
Freund's Adjuvant - toxicity
Immunologic Memory - physiology
Male
Memory cells
Myelin Basic Protein - immunology
Neurology
Rats
Rats, Inbred Lew
Rats, Sprague-Dawley
Sex Characteristics
Spleen - metabolism
Spleen - pathology
Time Factors
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Abstract Animals that have recovered from adoptively transferred EAE develop clinical disease signs 2–3 days earlier than controls when challenged with encephalitogen. This may be due to the reactivation of donor-derived memory cells or stimulation of recipient-derived memory cells primed during the adoptive disease episode. In order to determine the origin of the memory cell subset, we used a donor–recipient model where donor cells are rejected in recipients following a course of adoptively transferred disease. Our results suggest the early onset of disease seen in recipients recovered from adoptively transferred disease and challenged with encephalitogen is due to the sustained presence of donor-derived memory cells.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2014.11.006