To clarify hepatic immunological regulation under colitic conditions, we used three murine IBD models: (1) RAG-2−/− mice adoptively transferred with splenic CD4+CD45RBhigh T cells from wild-type (WT) mice [15]; (2) an acute dextran sulfate sodium (DSS)-induced colitis model [16]; and (3) IL-10−/− mice [17] that spontaneously develop chronic IBD-like colitis. Here, CD4 is linked to colitis.