Table 1 Formation of GAPs in the murine model is regulated throughout life by a variety of mechanisms to tightly control when exposure to luminal antigens occurs to prevent the development of inflammation to dietary antigens or the dissemination of potential pathogens. Bold indicates GAPs, and development of tolerance to GAP-delivered antigens. Underline indicates no GAPs, and potential of inflammation following GAP formation. Italics indicate no GAPs, and danger of increased pathogen dissemination following GAP formation
From: Goblet cells: multifaceted players in immunity at mucosal surfaces
| Â | Early life | Adult steady state | Infection | |
|---|---|---|---|---|
Small Intestine | GAPs? | No GAPs until DOL1856 | GAPs 54 | No GAPs 64 |
Regulation mechanism | Inhibited by luminal EGFR ligands before DOL 1056 | Can be inhibited by luminal EGFR ligands 29 | Inhibited by IL1β 64 | |
Consequence of antigen delivery | Unexplored | Unexplored | Inflammation to GAP-delivered antigens 64 | |
Colon | GAPs? | GAPs DOL10-weaning 56 | No GAPs 29 | No GAPs 64 |
Regulation mechanism | Inhibited by luminal EGFR ligands before DOL 10 56 | Inhibited by luminal TLR ligands from SPF housed microbiota 29 | Inhibited by luminal TLR ligands from SPF housed microbiota 64 | |
Consequence of antigen delivery | Tolerance to GAP-delivered antigens 56 | Increased dissemination of pathogens 64 | ||
Distal colon | GAPs? | Unexplored | GAPs 44 | Unexplored |
Regulation mechanism | Unexplored | Unexplored | Unexplored | |
Consequence of antigen delivery | Unexplored | Unexplored | Unexplored | |
