Figure 4.
Modulation of IL-6/STAT3 axis in Tcons is mediated by AZA and is independent of IL-6 receptor levels. (A) Representative flow cytometry histograms of a patient with CR and a patient who failed AZA gated on Tcons. (B) A significant downregulation of the IL-6/STAT3 node was already evident at day 15 of the first AZA cycle in patients who achieved CR (n = 6), whereas there was no modification in STAT3 phosphorylation in patients who failed treatment (n = 9). Data shown as mean ± standard error of the mean. (C) No differences in the expression of IL-6Rα in Tcons were observed between downregulators (n = 5) or upregulators (n = 5) either prior (P = .54) or after AZA (P = .94). Likewise, AZA therapy did not modify the expression of IL-6Rα in Tcons in both downregulators (P = .1) and upregulators (P = .18; i). Similar to IL-6Rα, gp130 expression was comparable between downregulators and upregulators both before (P = .22) and after AZA (P = .66), whereas AZA therapy did not alter significantly gp130 levels in Tcons in both downregulators (P = .31) and upregulators (P = .31; ii). *P < .05. CR, complete remission; UT, untreated/unmodulated node; NMFI, normalized median fluorescence intensity.