M2 macrophage

Byaibio

M2 macrophage, also called the M2 phenotype, is an immunosuppressive macrophage state that supports tumor progression by dampening anti-tumor immunity and promoting a pro-tumor microenvironment. It is often discussed as a polarized macrophage classification within the tumor microenvironment, where it can be linked to vascular invasion, persistent tumor burden, and worse survival in ovarian cancer. In bladder cancer, a hydrogel-mediated Bacillus Calmette-Guérin delivery strategy was reported to suppress the pro-tumorigenic M2 phenotype, highlighting a delivery-based approach to macrophage reprogramming. Recent studies also describe exosome-driven polarization toward M2-like macrophages and an IL-18-armed oncolytic vaccinia virus that remodels suppressive immune states by modulating macrophages and Tregs.

Tumor progression and immune suppression

  • Exosomes were reported to polarize macrophages toward the M2 phenotype in the tumor microenvironment, supporting tumor progression and immune evasion. (PMID:41759799)
  • The M2 state was described as an immunosuppressive macrophage subset increased in the tumor microenvironment in the study context. (PMID:42012649)
  • In ovarian cancer, M2-macrophages were associated with vascular invasion, persistent tumor, and worse survival. (PMID:42008432)
  • The entry’s key fact emphasizes suppression of the pro-tumorigenic M2 phenotype as a relevant therapeutic goal. (PMID:41936056)

Therapeutic modulation and delivery

  • A hydrogel-mediated BCG delivery strategy in bladder cancer suppressed the pro-tumorigenic M2 phenotype, suggesting local delivery can reshape macrophage polarization. (PMID:41936056)
  • An IL-18-armed oncolytic vaccinia virus was reported to remodel the suppressive microenvironment via macrophage and Treg modulation in lymphoma. (PMID:42012649)
  • The vaccinia-virus relation indicates this therapy targets macrophage polarization, including M2 macrophages. (PMID:42012649)
  • These findings support macrophage reprogramming, rather than direct depletion, as a mechanism for improving anti-tumor immunity. (PMID:41936056)