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. Author manuscript; available in PMC: 2013 Nov 10.
Published in final edited form as: Mucosal Immunol. 2010 Oct 20;4(1):10.1038/mi.2010.66. doi: 10.1038/mi.2010.66

Figure 1. Mucosal exposure to pathogens and host response.

Figure 1

The mucosal epithelium presents a formidable structural and chemical barrier to ill-intentioned microbes, which gain entry into the lamina propria (1) by dendritic cells, (2) through disrupted or injured epithelium, (3) between or through intact epithelial cells, and (4) through M cells. In noninflamed lamina propria, macrophages phagocytose and kill microbes without an inflammatory response. In the present of inflammation and dysregulated mucosal homeostasis, newly recruited monocyte-derived macrophages (and other innate host defense cells) generate transforming growth factor-β (TGF-β) and chemokines to recruit monocytes and other leukocyte populations to contain the infection. Microbes and/or their products are transported by dendritic cells in the lymphatics to draining lymph nodes where they induce an adaptive immune response. Failed clearance of the microbe and/or an inability to restore homeostatic regulation because of genetic and environmental factors can perpetuate inflammation locally and/or systemically (illustration by Lydia Kibiuk, NIH).