To evaluate the role of the IFNβ-JAK1/TYK2-STAT1-IRF7 pathway in lymphocyte migration during endotoxemia, we established an in vivo air pouch model and found that supernatants of BMDMs treated with MRP8/14 significantly enhanced the chemotaxis of white blood cells, whereas the supernatants of BMDMs treated with the IFNβ neutralizing Ab, GLPG0634 or fludarabine or from Irf7−/− mice failed to increase the chemotaxis of white blood cells into the air pouches (Figure 5g). The gene discussed is JAK1; the disease is serum lipopolysaccharide activity.