Skip to main content
. Author manuscript; available in PMC: 2011 Apr 1.
Published in final edited form as: J Immunol. 2010 Mar 1;184(7):3450–3460. doi: 10.4049/jimmunol.0903831

Figure 7. CXCL10/IP10 antagonizes the action of CXCL9 during priming of donor-reactive, IFN-γ-producing CD8 T cells.

Figure 7

(A) Spleens from wild-type or CXCL10−/− B6 recipients of wild-type or CXCL10−/− Balb/c heart allografts were harvested on day 7 post-transplant. CD8 or CD4 T cells were purified and the number of donor-specific cells producing IFN-γ was quantified using ELISPOT. (B) Flow sort purified naïve 2C CD8 T cells were cocultured with B6 spleen cells pulsed or not pulsed with 2C peptide for 3 days in the presence of anti-CXCL10 mAb (5 ug/mL) or control Ab and increasing amounts of recombinant CXCL9 as shown. 2C cells producing IFN-γ were then determined by intracellular cytokine staining. Data represents two independent experiments, 3 replicates/group; mean ± SEM. (C) CXCL10−/− allograft combinations were treated with control IgG or with anti-CXCL9 mAb (150ug, i.p., d1, 3, 5). The number of IFN-γ-producing CD4 or CD8 T cells was enumerated by ELISPOT on day 7 post-transplant. Data represents two independent experiments, n = 3/group; mean ± SEM, * p < 0.05, ** p < 0.01.