The effect of anti- TNF on the APR after focal cerebral ischemia. (A) Changes in liver CXCL10, CXCL1, CCL2, IL-1β, SAA2 and SAP mRNA levels after pMCAO (*P <0.05, **P <0.01, one-way ANOVA followed by Bonferroni post-hoc test, three to six per group). (B) Flow cytometry analysis of spleen samples six and 24 hours after pMCAO show a decrease in numbers of T-cells (CD45+CD3+) in XPro1595- and etanercept-treated mice 24 hours after pMCAO compared to non-lesioned mice. At 24 hours, the number of T-cells were decreased in etanercept-treated mice compared to saline-treated mice. The number of monocytes (CD11b+CD45highGr1−) was found to increase in XPro1595-treated mice at six hours and decrease at 24 hours, compared to non-lesioned mice. The number of granulocytes (CD11b+CD45highGr1+) was found to increase at six hours in all groups compared to non-lesioned mice, and to decrease at 24 hours in saline- and XPro1595-treated mice. (C) Flow cytometry analysis of blood samples showed that the number of T-cells increased at six hours in saline-treated, but not in XPro1595- and etanercept-treated mice, compared to non-lesioned mice. The total number of T-cells was increased in saline-treated mice compared to XPro1595- and etanercept-treated mice at six hours. At 24 hours, the total number of T-cells was decreased in all treatment groups. No change was observed at any time point in blood monocytes. The number of granulocytes was found to increase in blood in saline-treated mice at six hours compared to non-lesioned mice, but also compared to XPro1595- and etanercept-treated mice with six hours survival (*P <0.05, four to six per group). ANOVA, analysis of variance; APR, acute phase response; CCL, chemokine (C-C motif) ligand; CXCL, chemokine (C-X-C motif) ligand; IL, interleukin; pMCAO, permanent middle cerebral artery occlusion; SAA2, serum amyloid A2; SAP, serum amyloid P; TNF, tumor necrosis factor.