STAT3 is activated by many cytokines, including the IL-6 family of cytokines (Darnell, 1997). Stat3 null mice were embryonic lethal (Takeda et al., 1997). Conditional Stat3 knockouts using the Cre-loxP system have uncovered physiological roles of STAT3 in various tissues and cell types, including liver (Alonzi et al., 2001), T lymphocytes (Takeda et al., 1998), macrophages and neutrophils (Takeda et al., 1999), and bone marrows (Lee et al., 2002; Welte et al., 2003). These studies demonstrate that STAT3 participates in various cytokine signaling pathways and that STAT3 is important in cell proliferation, differentiation, migration, and apoptosis (Levy and Lee, 2002). For example, mice with Stat3 deletion in macrophages and neutrophils showed increased inflammatory responses and developed chronic colitis (Takeda et al., 1999). The deletion of Stat3 in T lymphocytes caused impaired IL-6-dependent cell survival (Takeda et al., 1998).

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