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23 Recently, attention has focused on the idea that a population of LP myeloid cells expressing the chemokine receptor CX3CR1 may be able to sample the intestinal lumen by extending cellular processes across the epithelial barrier 24 without perturbing tight junctions and epithelial integrity. 25 Although it has been speculated that these CX3CR1high cells might facilitate antigen uptake in vivo ( Figure 1), the frequency of transepithelial protrusions varies markedly between mouse strains and between the various segments of the intestine. 26, 27 Finally, our own and other work has shown that the CX3CR1high cells in LP do not appear to be bona fide DCs, as they do not migrate from LP to mLNs and cannot present luminal antigen to naive T cells. 28, 29, 30 Nevertheless, they do seem to be loaded efficiently with antigen and hence may play an accessory role, by passing it on to neighboring migratory DCs for transport and presentation. As discussed below, CX3CR1high cells may also be important for local differentiation of the Tregs needed to maintain oral tolerance.
CD11b monocytes may also play a role in the induction of Tregs, and the induction of Tregs occurs in the MLNs and involves both C-C motif receptor 7 (CCR7) and CCR9. Co-stimulation by PDL1-programmed cell death ligand (PDL) is also important for the induction of Tregs. Macrophages are stimulated to produce TGF-ß after uptaking apoptotic epithelial cells or apoptotic T cells following high-dose tolerance. Lower doses of antigen favor the induction of Tregs, whereas higher doses of antigen favor anergy / deletion as a mechanism of tolerance induction. The liver may also play a role in oral tolerance.
CD11b monocytes may also play a role in the induction of Tregs, and the induction of Tregs occurs in the MLNs and involves both CCR7 and CCR9. Costimulation by PDL1-PDL are also important for the induction of Tregs. Macrophages are stimulated to produce TGF-ß after uptaking apoptotic epithelial cells or apoptotic T cells following high dose tolerance. Lower doses of antigen favor the induction of Tregs, whereas higher doses of antigen favor anergy/deletion as a mechanism of tolerance induction. The liver may also play a role in oral tolerance.
Oral tolerance refers to a specific type of peripheral tolerance induced by antigens given by mouth and exposed to the gut mucosa and its associated lymphoid tissues.  The hypo-responsiveness induced by oral exposure is systemic, and can reduce hypersensitivity reactions in certain cases. Records from 1829 indicate that American Indians would reduce contact hypersensitivity from poison ivy by consuming leaves of related Rhus species; however, contemporary attempts to use oral tolerance to ameliorate autoimmune diseases like rheumatoid arthritis and other hypersensitivity reactions have been mixed.
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Tolerance induction is the default immune pathway in the gut, and the type of tolerance induced relates to the dose of antigen fed: anergy/deletion (high dose) or regulatory T-cell (Treg) induction (low dose). Conditioning of gut dendritic cells (DCs) by gut epithelial cells and the gut flora, which itself has a major influence on gut immunity, induces CD103+ retinoic acid-dependent DC that induces Tregs. A number of Tregs are induced at mucosal surfaces. Th3 type Tregs are transforming growth factor-β dependent and express latency-associated peptide (LAP) on their surface and were discovered in the context of oral tolerance.
Benson et al. (14) did not report the effect of their feeding regimen on humoral immunity, but one presumes that antibody responses were suppressed. They did, however, carry out detailed analysis of cytokine responses following a single high-dose feeding. They found that on day 1 there was an increase in the number of cells expressing IL-2, IFN-?, IL-5, and IL-4, followed by their subsequent decrease and apparent deletion by day 14, a consequence of apoptosis. Cells secreting TGF-ß, referred to as Th3 cells, have been implicated in the active suppression mechanism of oral tolerance.