Role for STAT3 in G-CSF–inducible CXCR2 expression. (A) WT and STAT3-deficient (KO) mice were treated with G-CSF (250 μg/kg; +G-CSF, bottom) or left untreated (−G-CSF, top) and bone marrow samples were isolated after 24 hours. CXCR2 expression in the Gr-1⁺ population is shown: WT (black line), KO (gray line). Isotype controls are included (dashed gray line). Data shown are from a representative experiment (n = at least 3 for each group). (B) The average percentage of CXCR2-positive cells within the bone marrow Gr-1^hi and Gr-1^lo subsets from untreated (−G-CSF) or G-CSF–treated (+G-CSF) WT and STAT3-deficient (KO) mice is shown (n = at least 3 for each group). (C) WT and STAT3-deficient (KO) mice were untreated or treated with G-CSF as indicated in panel A. Relative Il8rb mRNA levels were determined in purified Gr-1^lo and Gr-1^hi subsets, by comparison with the housekeeping gene Rpl13a. Shown are mean relative expression levels (n = at least 4). (D) WT and STAT3-deficient (KO) mice were untreated or treated with G-CSF as indicated in panel A. MIP-2–responsive chemotactic activity of purified immature Gr-1^lo and mature Gr-1^hi neutrophils was determined by Transwell assays. The average percentage of migrated cells/total cells is shown for each condition (n = 5 for each group). Error bars represent SEM; *P < .05, **P < .01, ***P < .001.