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. 2009 Mar 26;106(15):6232–6237. doi: 10.1073/pnas.0808144106

Fig. 4.

Fig. 4.

In vivo activated monocytes drive Th17 responses via a cell-contact dependent mechanisms. (A) The percentage of IL-17+CD4+ T cells (ICC, Left) and IL-17 production (ELISA, Right) induced by coculture of RA PB CD4+ T cells with autologous RA PB or SF-derived monocytes, or LPS-activated RA PB monocytes (mean ± SEM, n = 9). Statistical analysis was performed with a nonparametric matched pairs test (Wilcoxon). (B) RA PB CD4+ T cells were cultured with anti-CD3 mAb and in vivo activated monocytes in the presence or absence of neutralizing anti-IL-1β and anti-TNF-α mAbs (Abs), and analyzed by ICC (Left) and ELISA (Right) for IL-17. (C) Purified CD4+ T cells from PB of HC (n = 3) were cultured with autologous monocytes and anti-CD3 mAb in the lower compartment of a transwell system, with or without an insert containing CD14+ monocytes from PB, SF, or SM of a patient with active RA. The percentage of IL-17+ T cells and levels of IL-17 secretion in the bottom wells were measured by ICC (Left) and ELISA (Right). The experiment was repeated in an autologous system with cells from PB/SF of an independent RA patient with similar results.