Rheostat regulation of integrin-mediated leukocyte adhesion
J. Clin. Invest. Ivor S. Douglas, et al. 117:2391 doi:10.1172/JCI33376 [Go to this article.]

Figure 3
Activated α₄β₇⁺ T cells drive gut inflammation in IBD. (A) Barrier dysfunction of the follicular-associated epithelium may represent a crucial step in the initiation of gut inflammation. The sites of initial inflammation in IBD are the lymphoid follicles, in which the aphthoid lesions originate from small erosions of the follicular-associated epithelium (35, 36). In IBD, the expression of proinflammatory cytokines (e.g., TNF-α, IFN-γ, and IL-12) leads to endothelial cell activation and upregulation of the expression of MAdCAM-1 and other endothelial CAMs. (B) Greater numbers of activated gut-homing T cells migrate through the endothelium to the lamina propria and the epithelium, where they are involved in tissue injury.