Figure 3
Induction of interleukin (IL)-10 and type 1 regulatory T cells contributes to the inhibitory effect of Neisseria gonorrhoeae (Ngo) on development of BALB/c mouse T helper type 1 (Th1) and Th2 cells, and blockade of these mechanisms promotes Th1 and Th2 as well as Th17 responses. (a) Suppression of cell proliferation in Th1- and Th2-polarized CD4+ cell cultures by N. gonorrhoeae (multiplicity of infection (MOI) 50:1) was reversed by treatment with anti-IL-10 (40 μg ml−1) or/and transforming growth factor-β (TGF-β) antibody (40 μg ml−1). The sequential loss of CFSE (carboxymethyl fluorescein succinimide ester) fluorescence was used to measure cell proliferation. (b) Suppression of interferon (IFN)-γ and IL-5 production in Th1- and Th2-polarized CD4+ cell cultures, respectively, by N. gonorrhoeae (MOI 50:1) was reversed by treatment with anti-IL-10 or/and TGF-β antibody. (c) Effect of anti-IL-10 antibody alone or in combination with anti-TGF-β antibody on cytokine response of iliac lymph node (ILN) cells stimulated with N. gonorrhoeae (MOI 10:1) for 4 days. (d) Effect of anti-IL-10 antibody alone or in combination with anti-TGF-β antibody on expression of T-bet, GATA3, and RORγt (retinoic acid–related orphan receptor γt) in CD4+ T cells MACS (magnetic-activated cell sorter)-purified from ILN cultures stimulated with N. gonorrhoeae (MOI 10:1) for 4 days. Transcription factor gene expression levels detected by reverse transcriptase–PCR were normalized relative to expression of β-actin and set at 1.0 for unstimulated cells. All data shown are representative of four independent experiments. #P<0.05; *P<0.01 anti-IL-10 vs. control immunoglobulin G (IgG) treatments or anti-IL-10 plus anti-TGF-β vs. anti-IL-10 treatments.
