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. 2009 May;20(5):1032–1040. doi: 10.1681/ASN.2008070778

Figure 6.

Figure 6.

Inflammatory cytokines augment T cell proliferation in an IRAK-M–dependent manner. IRAK-M−/− transplant recipients resist the graft-prolonging effects of anti-CD45RB and anti-CD154 to extend allograft survival. (A) WT and IRAK-M−/− macrophages were stimulated with LPS, and CM were harvested. These media were used to culture T cells that were stimulated with allogeneic APCs. IRAK-M−/− CM augmented T cell alloimmune proliferation versus WT CM (*P < 0.05). This difference was blocked by either IL-6 or TNF-α inhibition. (B) C57BL/6 IRAK-M−/− recipients of BALB/c skin allografts that were treated perioperatively with anti-CD45RB and anti-CD154 rejected their allografts at a faster rate than similarly treated WT recipients (P = 0.03, log rank). Both groups rejected their allografts at a similar rate when co-stimulatory blockade was not administered (data not shown). (C) Bulk purified T cells from recipient mice in B were harvested 21 d after transplantation and were re-stimulated with irradiated BALB/c or third-party CBA (H2K) APCs. IFN-γ response was then measured via ELISPOT. T cells from IRAK-M−/− recipients exhibited an enhanced donor-specific IFN-γ versus WT recipients (P = 0.03; n = 3 per group, two independent experiments).