Modulation of oral tolerance

If oral tolerance is broadly defined as the inhibition of T||l responses in the periphery either by large doses of antigen that induce anergy or deletion or by gut-induced TH2- or TH3-type regulatory cells, anything that favors TH1 versus TH2 responses would abrogate oral tolerance and the converse (Table 3). Thus, large doses of IFNy abrogate oral tolerance and similar results would be expected with IL-12. Indeed investigators have found that anti-IL-12 enhances oral tolerance in OVA TCR transgenic animals and is associated with increased TGF|3 secretion. In the uveitis model, IL-2 potentiates oral tolerance and is associated with increased production of TGF|3, IL-4 and IL-10 in Peyer's patches. We have recently found that IL-4 administration enhances low-dose oral tolerance to MBP in the EAE model. Lipopolysaccharide (LPS) enhances oral tolerance to MBP and is associated with increased expression of IL-4 in the brain, and IFN|3 synergizes with the induction of oral tolerance in SJL/J mice fed low doses of MBP.

Cholera toxin (CT) is one of the most potent

Table 3 Modulation of oral tolerance



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