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. Author manuscript; available in PMC: 2016 Nov 28.
Published in final edited form as: Am J Transplant. 2015 Jun 16;15(9):2336–2345. doi: 10.1111/ajt.13350

Figure 3. Hyperlipidemia promotes an IL-17 mediated rejection response.

Figure 3

(A) Fold change in serum levels of proinflammatory cytokines were determined in C57BL/6 mice fed normal chow (white bars) or high-fat diet (black bars), ApoE−/− fed normal chow (gray bars) or a high-fat diet (lined bars) for 4 weeks that received a bm12 heart transplant. Serum was collected at the time of rejection, or at 100 days. Pooled serum from 4 to 6 mice was analyzed by Multiplex Elisa. (B) Absolute number of CD4 cells producing IL-17 or IFN-γ in the lymph nodes of C57BL/6 fed normal chow (white bars) or ApoE−/− mice fed a high-fat diet (black bars) that received a bm12 heart transplant as determined by flow cytometry. Untransplanted ApoE−/− mice on a high-fat diet (gray bars) were used as controls. n = 3–6 mice per group. Asterisk indicates p < 0.05. (C) Fold change in the frequency of CD4 T cells expressing IL-17 in the spleen was determined in ApoE−/− mice fed normal chow (gray bars) or a high-fat diet (black bars) and C57BL/6 mice fed normal chow (horizontal lines) or high-fat diet (diagonal lines) at the time of rejection of bm12 cardiac grafts, or at 100 days. Splenocytes were restimulated with PMA/ionomycin, and assayed for expression of IL-17 by intracellular staining and flow cytometry. Frequencies in naïve C57BL/6 mice (white bar) were used as an inter-experimental control. Asterisk indicates p value <0.05 relative to control. ApoE, apolipoproteinE; IFN-g, interferon gamma; IL, interleukin; PMA, phorbol myristate acetate.