Induction of experimental autoimmune neuritis in CD4(-)8(-) C57BL/6J mice

Citation
J. Zhu et al., Induction of experimental autoimmune neuritis in CD4(-)8(-) C57BL/6J mice, J NEUROIMM, 94(1-2), 1999, pp. 196-203
Citations number
33
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROIMMUNOLOGY
ISSN journal
01655728 → ACNP
Volume
94
Issue
1-2
Year of publication
1999
Pages
196 - 203
Database
ISI
SICI code
0165-5728(19990201)94:1-2<196:IOEANI>2.0.ZU;2-Q
Abstract
The C57BL/6J mice strain is known to be reputedly resistant to induction of experimental autoimmune neuritis (EAN), an animal model of Guillain-Barre syndrome in humans. Here we describe the induction of EAN in mice of the C5 7BL/6J background by transfer into naive syngeneic recipients bovine periph eral nerve myelin (BPM)-primed donor lymph node cells that had been stimula ted in vitro with the bovine peripheral nervous system (PNS) myelin P2 prot ein peptide 57-81 followed by challenge with BPM, Freund's complete adjuvan t and pertussis toxin. EAN was more severe, both clinically and histologica lly, and accompanied by extensive infiltration of inflammatory cells and de myelination in peripheral nerves when examined on day 30 after transfer of primed T cells from CD4(-)8(-) mice into identical naive hosts than after t ransfer of cells from primed wild type, CD4(-)/(-) or CD8(-)/(-) mice to co rresponding recipient animals. EAN in CD4(-)8(-) mice was also associated w ith elevated numbers of P2 peptide-reactive interferon-gamma (IFN-gamma) se creting cells and alpha beta T cells were present in lymph nodes and spleen s. The data suggest that PNS myelin activated T cells from an EAN-resistant mice strain are capable of homing to the PNS. The expanded CD4(-)8(-) alph a beta T cells may have helper and effector functions, related to initiatio n of EAN in the CD4(-)8(-) mice. Lack of CD4(+) and CD8(+) expressing cells does not prevent the initiation of an autoimmune disease. (C) 1999 Elsevie r Science B.V. All rights reserved.