Suppression of experimental autoimmune encephalomyelitis by oral administration of myelin basic protein and its fragments

@article{Higgins1987SuppressionOE,
  title={Suppression of experimental autoimmune encephalomyelitis by oral administration of myelin basic protein and its fragments},
  author={Paul J. Higgins and Howard L. Weiner},
  journal={Journal of Neuroimmunology},
  year={1987},
  volume={16}
}
  • P. Higgins, H. Weiner
  • Published 1 September 1987
  • Medicine, Biology, Psychology
  • Journal of Neuroimmunology
Oral Tolerance in Autoimmune Encephalomyelitis.
TLDR
The results suggest that there is an anergy component to low-dose oral tolerance and that deletion of MBP-reactive T cells accompanies high- dose oral tolerance.
Oral administration of myelin basic protein is superior to myelin in suppressing established relapsing experimental autoimmune encephalomyelitis.
TLDR
Oral administration of high doses of myelin, either before disease induction or during REAE, did not provide protection from disease or decrease in vitro T cell responses, and Ag homogeneity is also important, i.e., homogeneous Ag (MBP) is more effective at inducing oral tolerance than heterogeneity Ag (myelin).
Acquired tolerance to experimental autoimmune encephalomyelitis by intrathymic injection of myelin basic protein or its major encephalitogenic peptide
TLDR
The results indicate that the thymus may play an active role in acquired systemic immunologic tolerance in T cell-mediated experimental autoimmune diseases.
Tolerance Induction and Autoimmune Encephalomyelitis Amelioration After Administration of Myelin Basic Protein–derived Peptide
TLDR
It is proposed that continuous encounters of MBP-specific T cells with p17 play a critical role in the induction and maintenance of tolerance, and seems to be based on reduction in the responsiveness of anti-MBP T cells.
Suppression of Experimental Autoimmune Encephalomyelitis in the Rat by Oral Administration of Spinal Cord Protein Hydrolysate
TLDR
Application of the oral toleration method using myelin proteins or their components gives the possibility for a decrease in the number of autoimmunologic reactions, and some studies show that the primary mechanism of oral tolerance is generation of active suppression.
Oral tolerance as therapy for experimental autoimmune encephalomyelitis and multiple sclerosis: Demonstration of T cell anergy
TLDR
Clonal anergy as an important mechanism for oral tolerance is supported after T cells derived from MBP‐fed rats underwent a dramatic reversal of unresponsiveness, proliferate in response to MBP and are capable of transferring EAE.
Orally administered myelin basic protein in neonates primes for immune responses and enhances experimental autoimmune encephalomyelitis in adult animals
TLDR
Results suggest that immaturity of the immunoregulatory network associated with oral tolerance and sensitization to autoantigens via the gut in the neonatal period may contribute to the pathogenesis of autoimmune diseases.
Mechanisms of suppression of experimental autoimmune encephalomyelitis by intravenous administration of myelin basic protein: role of regulatory spleen cells.
TLDR
The results suggest that reversal of clinical EAE by iv injection of MBP at the time of disease onset is due at least in part to a T cell control mechanism located in the spleen and suggest the presence of splenocyte regulatory cells that can suppress the ability of encephalitogenic T cells to induce EAE.
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