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.

		Early life	Adult Steady State	Infection
Small Intestine	GAPs?	No GAPs until DOL18 65	GAPs 63	No GAPs 73
	Regulation Mechanism	Inhibited by luminal EGFR ligands before DOL 10 65	Can be inhibited by luminal EGFR ligands 37	Inhibited by IL1β 73
	Consequence of Antigen delivery	Unexplored	Tolerance to GAP delivered antigens 37	Inflammation to GAP delivered antigens 73
Colon	GAPs?	GAPs DOL10-weaning 65	No GAPs 37	No GAPs 73
	Regulation Mechanism	Inhibited by luminal EGFR ligands before DOL 10 65	Inhibited by luminal TLR ligands from SPF housed microbiota 37	Inhibited by luminal TLR ligands from SPF housed microbiota 73
	Consequence of Antigen delivery	Tolerance to GAP delivered antigens 65	Inflammation to GAP delivered antigens 37,65	Increased dissemination of pathogens 73
Distal colon	GAPs?	Unexplored	GAPs 53	Unexplored
	Regulation Mechanism	Unexplored	Unexplored	Unexplored
	Consequence of Antigen delivery	Unexplored	Unexplored	Unexplored

Green indicates GAPs, and development of tolerance to GAP delivered antigens

Orange indicates no GAPs, and potential of inflammation following GAP formation.

Red indicates no GAPs, and danger of increased pathogen dissemination following GAP formation.