In article <p_travers-170194134814 at macmhc.cryst.bbk.ac.uk> p_travers at icrf.icnet.uk (Paul J Travers) writes:
> TI: Inhibition of experimental autoimmune encephalomyelitis by
> but not oral administration of the encephalitogenic peptide:
> Influence of MHC binding affinity
> AU: Metzler_B, Wraith_DC
> JN: International Immunology 1993 Vol.5 No.9 pp.1159-1165 ). And
>the use of (re)stimulation with Ag in CFA and whether the adjuvant
>overrides any hyporesponsiveness set up by oral administration of antigen.
>Has your lab looked at stimulating with Ag in IFA to see if there is a
>difference between fed and unfed animals?
In EAU, Ag/IFA does not induce disease, CFA is necessary. Therefore since we
want to study inhibition of disease we use AG/CFA. We haven't checked any
other adjuvants. The results show that oral tolerance inhibits disease
induced by Ag/CFA, but as always, inhibition is never 100%. So it's possible
that CFA-induced inflammation might override some of the tolerance, but in
general, the tolerance mechanism seems to control the inflammation.
The Ag/IFA is an interesting idea however, perhaps the non-pathogenic T cells
(specific for the immunizing bovine Ag, not the target rat Ag) might be
stimulated by this.