Fig. 1

a C-RP in baboons with pig artery patch (n = 9) or organ (n = 17) grafts. Levels of C-RP in baboons before (day 0) and after pig organ or artery patch transplantation. (Black line = without tocilizumab therapy; Red line = with tocilizumab therapy.) The mean level of C-RP in the tocilizumab-treated baboons remained < 0.5 mg/dL from day 4, which (on days 7, 14, 28, and 60) was significantly lower than in baboons not receiving tocilizumab (day 7, 0.2 vs 1.6 mg/dL, P < 0.001; day 14, 0.3 vs 1.8 mg/dL, P < 0.001; day 28, 0.3 vs 1.6 mg/dL, P < 0.001; and day 60, 0.3 vs 2.0 mg/dL, P < 0.01, respectively). (**P < 0.01; ***P < 0.001). Tocilizumab treatment therefore prevented an increase in C-RP after xenotransplantation. (The rise in C-RP on day 136 in one of the baboons in the tocilizumab-treatment group was associated with the onset of systemic infection.) (Reprinted with permission from ref. [26]). b C-RP deposition in pig kidneys transplanted into baboons, an indicator of the inflammatory response to the graft. (Left panel) At 30 min after reperfusion of an α1,3-galactosyltransferase gene-knockout (GTKO) pig kidney graft, no C-RP deposition was detected. In two different kidneys at the time of euthanasia (middle and right panels), C-RP deposition was detected in the glomeruli (arrow heads, right panel) and tubules (arrows, middle and right panels). Our data suggest that both the xenograft and the recipient contribute to C-RP production. (We detected minimal C-RP in NHPs undergoing heart allotransplantation [not shown]). (Reproduced with permission from ref. [18])