Model illustrating the roles of the Toll-like receptor (TLR) and Stat3 in IBD. Myeloid cells respond to LPS-mediated TLR stimulation. Normally, inflammation is controlled by IL-10, which stimulates myeloid cell Stat3 activation to suppress TLR-induced IL-12/IL-23 production (a). Kobayashi et al. (7) demonstrate that in LysMCre/Stat3^flox– mice, IL-10 does not effectively suppress IL-12/IL-23 production. IL-12/IL-23 release activates lymphocytes, causing an exaggerated bias toward Th1-type inflammation (b).