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. 2000 Nov 20;192(10):1515–1520. doi: 10.1084/jem.192.10.1515

Figure 3.

Figure 3

In vitro and in vivo effects of CXCR3 targeting. (a) CXCR3−/− knockout (KO) mice have (a) normal mitogen responses but (b) diminished alloreactivity (MLR); bars show the mean ± SD for 12 wells. Asterisks indicate significantly decreased proliferation compared with wild-type (WT) responses (P < 0.001, Mann-Whitney U test). (c) Dose-dependent inhibition of MLR by anti-CXCR3 mAb; bars indicate the mean ± SD for 12 wells, mAb final concentrations expressed in μg/ml. Asterisks indicate significantly decreased proliferation using CXCR3 mAb compared with cells treated with IgM (*P < 0.005, **P < 0.001, Mann-Whitney U test). (d) Prolongation of cardiac allograft survival in knockout versus wild-type recipients, and permanent engraftment when knockout recipients received 14 d of CsA. Bars indicate the mean ± SD for six mice. Asterisks indicate significantly increased prolongation of allograft survival compared with the respective control group (P < 0.001, Mann-Whitney U test). (e) Anti-CXCR3 mAb prolongs cardiac graft survival whether begun pretransplant (day 0) or once rejection has begun (day 4); bars indicate the mean ± SD for six mice. Asterisks indicate significantly increased prolongation of allograft survival compared with the respective control group (P < 0.001, Mann-Whitney U test).