The Genetics of Inflammatory Bowel Disease Judy H. Cho, Casey T. Weaver  Gastroenterology  Volume 133, Issue 4, Pages 1327-1339 (October 2007) DOI: 10.1053/j.gastro.2007.08.032 Copyright © 2007 AGA Institute Terms and Conditions

Figure 1 Spectrum of CD susceptibility alleles. Minor allele frequencies are plotted as a function of allelic odds ratios for the most well-established CD susceptibility alleles. With the exception of the NOD2 risk alleles, functional studies establishing a direct pathogenic role have not been performed, and the plotted odds ratios represent estimates of representative, associated markers. The NOD2 risk alleles are estimated from a population-based cohort from Manitoba.32 Gastroenterology 2007 133, 1327-1339DOI: (10.1053/j.gastro.2007.08.032) Copyright © 2007 AGA Institute Terms and Conditions

Figure 2 (A) CD4 T-cell effector development. This schematic highlights key inductive and effector cytokines associated with the development and function of the Th1, Th2, and Th17 lineages in mice. TN, naive CD4 T cell. (B) Developmental divergence of the Th1 and Th17 lineages. This schematic highlights key cytokines, signaling components, and transcription factors that distinguish Th1 and Th17 development (see text for details). TN, naive CD4 T cell. (C) Shown are the key receptors and ligands expressed by naïve T, Th17, and Th1 cells. Structural homology between the IL-6, IL-12, IL-23, and IL-27 receptors is evident, including the shared component of the IL-6 and IL-27 receptors, gp130. The IL-6 and IL-27 receptors are expressed by naive T cells, as is the IL-12Rβ1 chain that is common to the IL-12 and IL-23 receptors. The inducible chain of the IL-23 receptor, IL-23R, is expressed downstream of Th17 lineage commitment. Activation of the principal STATs, believed to be important in Th17 and Th1 differentiation, is indicated in black; other STATs recruited by these receptors are indicated in gray. (D) Positive and negative regulators of Th17 development. This schematic highlights key cytokines that promote or inhibit Th17 development. Gastroenterology 2007 133, 1327-1339DOI: (10.1053/j.gastro.2007.08.032) Copyright © 2007 AGA Institute Terms and Conditions