Research Paper Volume 14, Issue 15 pp 6149—6168

Figure 6. IL-17D promotes TAM infiltration via the p38 MAPK signaling pathway in lung cancer. (A and B) The relative mRNA levels of genes related to macrophages recruitment and polarization were measured via quantitative real-time polymerase chain reaction. RNA was purified from A549 cells expressing IL-17D treated with SB203580, IL-17D treated with DMSO, or empty vector treated with DMSO (A). RNA was purified from LLC1 cells expressing IL-17D treated with SB203580, IL-17D treated with DMSO, or empty vector treated with DMSO (B). Mean ± SD. ^*P < 0.05. ^**P < 0.01. (C) Representative images of recruited macrophages. Scale bars, 100 μm. (D) Quantification of recruited macrophages. Mean ± SD. ^***P < 0.001. (E) Proposed model for mechanism of IL-17D inducing TAMs infiltration into the TME. High expression of IL-17D in lung cancer cells activates p38 MAPK signaling pathway through binding to receptor complexes of lung cancer cells, which upregulates TAM recruitment– and polarization–related genes expression and promotes infiltration of TAMs in lung cancer.