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. 2021 Oct;10(10):4012–4026. doi: 10.21037/tlcr-21-465

Figure 2.

Figure 2

M2 polarization of macrophages induced by Mycobacterium tuberculosis (MTB) in lung cancer (LC): macrophages are generally categorized to M1 or M2 phenotype. M1-like macrophages, induced by Th1 cytokines such as colony stimulating factor (CSF)-2, TNF-α, and IFN-γ, are associate with pro-inflammatory and response against infected pathogens and cancer cells through ROS, TNF-α, IL-6, NO, etc. M2-like macrophages, induced by Th2 cytokines such as IL-4 and IL-13, contribute to angiogenesis and increased expression of immunosuppressive molecules to promote tumor cell growth, invasion, metastases. The M2 phenotype dominates in the intermediate and late phases of tuberculosis (TB), and raised levels of type-2 inflammatory response signals such as IL-4, IL-13 or IL-10 raised in TB patients, leading to the occurrence and progression of LC. MTB develops a relevant strategy to block M1 polarization through IL-6 involved bystander effect-mediated inhibition of the transcription of IFN-γ. While combining anti-Her2/neu antibody with targeted delivery of can skew M2-like macrophages to M1 phenotypes, and anti-TB therapy can shift the inflammatory atmosphere type-2 back to type-1, thus increase M1-like macrophages in PTB patients.