Figure 6.
M2 macrophage increased MCL growth via STAT1 signaling. STAT1, STAT3, ERK, and p65 phosphorylation in Granta (A) and Mino (B) cells was measured after direct or indirect coculturing with THP-1-Mφ with or without IL-10 neutralizing antibody. (C) Immunofluorescence staining showing CD19 and p-STAT1 staining in the Mino or Mino + CD14 inoculated MCL xenograft tumors (n = 3). (D) Cell proliferation in Mino and Granta was measured by MTT assay after coculturing with THP-1-Mφ with or without IL-10 neutralizing antibody. Cell proliferation in Mino and Granta was measured by MTT assay after direct or indirect coculturing with THP-1-Mφ with or without STAT1 and STAT3 inhibitor (E) or STAT1 and STAT3 shRNA (F). Data are presented as mean ± standard deviation from 3 separate experiments. *P < .05. GAPDH, glyceraldehyde-3-phosphate dehydrogenase.

M2 macrophage increased MCL growth via STAT1 signaling. STAT1, STAT3, ERK, and p65 phosphorylation in Granta (A) and Mino (B) cells was measured after direct or indirect coculturing with THP-1-Mφ with or without IL-10 neutralizing antibody. (C) Immunofluorescence staining showing CD19 and p-STAT1 staining in the Mino or Mino + CD14 inoculated MCL xenograft tumors (n = 3). (D) Cell proliferation in Mino and Granta was measured by MTT assay after coculturing with THP-1-Mφ with or without IL-10 neutralizing antibody. Cell proliferation in Mino and Granta was measured by MTT assay after direct or indirect coculturing with THP-1-Mφ with or without STAT1 and STAT3 inhibitor (E) or STAT1 and STAT3 shRNA (F). Data are presented as mean ± standard deviation from 3 separate experiments. *P < .05. GAPDH, glyceraldehyde-3-phosphate dehydrogenase.

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