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. 2017 Aug 28;8:1037. doi: 10.3389/fimmu.2017.01037

Figure 2.

Figure 2

Sirtuin 2 (SIRT2) deficiency does not affect proliferation and cytokine response of splenocytes and IFNγ production in mice challenged with toxic shock syndrome toxin-1 (TSST-1). (A,B) SIRT2+/+ and SIRT2−/− splenocytes were incubated for 48 h with lipopolysaccharide (LPS) (5 µg/ml), CpG (2 µg/ml), concanavalin A (5 µg/ml), anti-CD3/CD28 antibodies (1 µg/ml), phytohemagglutinin (PHA) (10 µg/ml), TSST-1 (2 µg/ml), and staphylococcal enterotoxin B (SEB) (5 µg/ml). Proliferation was measured by 3H-thymidine incorporation (A) while IL-2 and IFNγ concentrations in cell culture supernatants were quantified by ELISA (B). Data are means ± SD of triplicate samples from one experiment performed with four mice and are representative of two experiments (*P < 0.05). (C) SIRT2+/+ and SIRT2−/− mice (n = 8 per group) were injected with TSST-1 (0.5 mg/kg i.p.). Blood was collected after 0, 8, and 24 h to quantify IFNγ concentrations. Data are means ± SD. P > 0.5 for all time points. (D) SIRT2+/+ and SIRT2−/− splenocytes were incubated for 48 h with LPS, CpG, concanavalin A, anti-CD3/CD28 antibodies, PHA, TSST-1, and SEB. TNF, IL-6, IL-10, IL-12p70, CCL3 (MIP-1α), CCL4 (MIP-1β), and CCL5 (RANTES) were quantified by Luminex. Data (in pg/ml) are means ± SD of one experiment performed with three mice. CCL3 values in response to anti-CD3/CD8 were over the upper limit of detection of the assay (*P < 0.05).