Jci_page_head_homepage_01 Jci_page_head_homepage_02
Warren Strober, Kazuhiko Nakamura, Atsushi Kitani
Published in Volume 107, Issue 6
J Clin Invest. 2001; 107(6):667–670 doi:10.1172/JCI12559
Full text | PDF
Options: View larger image (or click on image)
Medium
Figure 1

Routes to mucosal inflammation. Antigens stimulating the mucosal immune system are presented via dendritic cells (DC; light blue) in the Peyer’s patches. In response, effector T cells (red) produce either IL-4 or IFN-γ and provide defense, whereas regulatory T cells (yellow) produce IL-10 and/or TGF-β and regulate the effector cells. In the normal, uninflamed intestine, the responses by effector cells and regulatory cells are balanced. T-cell development under these conditions (top panel) allows for host defense without inflammation. In the generalized model of mucosal inflammation, type 1 (middle panel), genetic factors lead to an excessive effector cell response that overwhelms or inhibits regulatory responses; inflammation ensues. Conversely, in the generalized model of mucosal inflammation, type 2 (bottom panel), the effector response is intrinsically normal but genetic factors lead to an attenuated regulatory response and, once again, to inflammation. While certain genetic factors must be present for disease to develop, environmental triggers must also be present to bring these genetic factors into play.