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. 2016 May 19;11(5):e0155870. doi: 10.1371/journal.pone.0155870

Fig 6. Natural killer cells do not contribute to enhanced T helper cell priming mediated by dendritic cells in the injured muscle.

Fig 6

(A) Schematic overview on the experimental setup. Natural killer (NK) cells were depleted through intraperitoneal application of anti–asialo ganglioside-monosialic acid (αGM-1) serum 24 h before and 48 and 96 h after injury or sham treatment. Normal rabbit serum (NRS) served as a control. All mice received ovalbumin (OVA)-specific T cells from DO11.10 mice intravenously (i.v.) 1 day before OVA application. Unlabeled lipopolysaccharide-containing OVA (Sigma) was injected intramuscularly (i.m.) into the gastrocnemius muscles 7 days after injury or sham treatment. After 3 days, the popliteal lymph node (pLN) cells were pooled by group and were stained with antibodies against CD49b or were restimulated with OVA peptide (pOVA). The content of interferon (IFN) γ in the supernatants was determined 3 days later. (B) Representative dot plots with numbers indicating the percentage of CD49b+ NK cells among popliteal lymph node cells. (C) Release of IFN-γ from restimulated lymph node cells. Data are presented as mean±SD of triplicate cultures and are representative of 2 experiments with n = 3 mice per group. Statistically significant differences were detected with two-way analysis of variance (ANOVA). *, p<0.05; **, p<0.01.