Protection from experimental autoimmune encephalomyelitis (EAE): non-depleting anti-CD4 mAb treatment induces peripheral T-cell tolerance to MBP in PL/J mice

Following pre-treatment with a non-depleting anti-CD4 mAb (H129.19) that produces long-lasting receptor saturation, PL/J mice were fully protected from experimental auto-immune encephalomyelitis (EAE) induced by injection of myelin basic protein (MBP). These mice did not develop EAE following MBP re...

Full description

Saved in:
Bibliographic Details
Published in:Journal of neuroimmunology 1997-03, Vol.73 (1), p.117-123
Main Authors: Biasi, G, Facchinetti, A, Monastra, G, Mezzalira, S, Sivieri, S, Tavolato, B, Gallo, P
Format: Article
Language:English
Subjects:
Animals
Anti-CD4 mAb
Antibodies, Monoclonal - immunology
CD4 Antigens - immunology
Disease Susceptibility
Drug Tolerance
EAE
Encephalomyelitis, Autoimmune, Experimental - immunology
Encephalomyelitis, Autoimmune, Experimental - prevention & control
Enterotoxins - immunology
Female
Immune Tolerance
Mice
Mice, Inbred Strains
Myelin Basic Protein - immunology
SEB
T-Lymphocytes - drug effects
T-Lymphocytes - pathology
Thymectomy
Thymus Gland - cytology
Thymus Gland - immunology
Tolerance
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:Following pre-treatment with a non-depleting anti-CD4 mAb (H129.19) that produces long-lasting receptor saturation, PL/J mice were fully protected from experimental auto-immune encephalomyelitis (EAE) induced by injection of myelin basic protein (MBP). These mice did not develop EAE following MBP re-challenge 5–10 weeks later when the CD4 + cells were no longer coated by the mAb and their lymph node cells were specifically unresponsive to MBP stimulation in vitro. Moreover, superantigen staphylococcal enterotoxin B (SEB) inoculation, which re-induces EAE in MBP immunized mice, failed to activate encephalitogenic T-cells in anti-CD4+MBP treated mice, even after MBP re-challenge, indicating that tolerance in the peripheral T-cell compartment was achieved. However, MBP re-challenge 16 weeks later, but not SEB, produced an acute episode of EAE in these mice, while it failed to induce disease in a parallel group of adult thymectomized mice. These results indicate that no memory of the first priming exists at this time and that new MBP-specific T-cell precursors are peripheralized and produce EAE after MBP recognition.
ISSN:0165-5728
1872-8421
DOI:10.1016/S0165-5728(96)00188-9