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. 2012 Oct 12;109(45):18535–18540. doi: 10.1073/pnas.1119133109

Fig. 6.

Fig. 6.

The loss of IL-27 responsiveness in CD8+ memory T cells reflects gp130 down-regulation. (A) C57BL/6 mice were infected with Sendai virus and, 30–45 d later, splenocytes were harvested and analyzed by flow cytometry. Expression of the IL-27Rα chain was assessed by pulsing cells with recombinant IL-27 on ice and measuring bound cytokine with an anti-IL-27 Ab. Control cells were held on ice without IL-27 and otherwise stained identically. (B) Splenocytes from C57BL/6 mice infected with Sendai virus 30–45 d earlier were stained with a gp130 mAb or an isotype-matched control (rat IgG2a) and analyzed by flow cytometry. (C) Splenocytes from C57BL/6 mice infected with Sendai virus 30–45 d earlier were harvested, cultured with or without IL-6, and analyzed by flow cytometry to assess STAT3 phosphorylation. In all panels, data are gated on CD8+ naïve (CD44lo) or Sendai-specific memory (CD44hi SenNP+) lymphocytes from the same spleen. Graphs depict mean fluorescence intensity (MFI) and each data point represents an individual mouse. All panels are representative of five mice per group in three or four independent experiments.