Skip to main content
. 2009 Mar;20(3):535–544. doi: 10.1681/ASN.2008040377

Figure 4.

Figure 4.

dDC and their importance in the induction of tolerance. (A) Whereas recipients of CX3CR1−/− hearts exhibited refractoriness to the effect of MR1, hearts from WT donors exhibited long-term allograft survival (MST of 20 and >100 d, respectively; n = 5 mice/group; P < 0.01). Hearts from CX3CR1−/− implanted with the Flt3L hybridoma exhibited restoration of prolongation of heart allograft survival by MR1 (MST >100; n = 5 mice; P < 0.1). Compared with WT donors treated with MR1, treatment of WT donors with Flt3L had no effect on the course of MR1 treatment (MST >100 d in both groups). To provide a suggestive mechanism for the necessity of tissue DC, we also co-transplanted hearts from WT and CX3CR1−/− mice into BALB/c recipients treated with MR1. (B and C) Both WT (B) and CX3CR1−/− (C) heart allografts showed preserved muscles with mild cellular infiltrates, although CX3CR1−/− hearts seem to have more dense infiltration (C). (D) Of note, single CX3CR1−/− heart allografts under MR1 showed massive infiltration with muscle necrosis, whereas WT allografts showed little inflammation and intact myocytes (data not shown).