After closure, any IgG localized in the lamina propria, whether from systemic sources or from uptake from the intestinal lumen, could contribute to proinflammatory responses in the intestine [158] . Indeed, post-closure uptake of IgG can occur via the FcRn receptor. FcRn has been identified in the human adult intestine [175, 176] , consistent with the hypothesis that FcRn is involved in IgG recycling (discussed in section 5.1). However, the transport of IgG across the enterocyte seems to be bidirectional, lending support to the concept that IgG in the intestine is involved in immune surveillance and defense of the mucosal lining [176] [177] [178] . Intestinal FcRn may deliver IgG-antigen immune complexes to the lamina propria for immune processing [158, 177] , thereby enhancing local mucosal immune response.