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Area of Science:

  • Immunology
  • Cell Biology
  • Pathology

Background:

  • Macrophages are innate immune cells with high plasticity.
  • They adopt context-dependent phenotypes influenced by origin and microenvironment, moving beyond discrete M1/M2 states.
  • This plasticity is crucial in various diseases.

Purpose of the Study:

  • To review molecular mechanisms shaping macrophage identity.
  • To explore macrophage plasticity across a spectrum of diseases.
  • To discuss emerging biomarkers and therapeutic strategies.

Main Methods:

  • Review of molecular circuits including TLR/cytokine signaling, microRNA networks, metabolic rewiring, and epigenetic mechanisms like histone lactylation.
  • Analysis of monocyte subset contributions to tissue macrophage diversity.
  • Examination of high-dimensional flow cytometry and mass cytometry (CyTOF) for integrated phenotyping.

Main Results:

  • Macrophage pathogenic phenotypes are context-dependent (e.g., M2-like TAMs in cancer vs. M1 in autoimmunity).
  • Soluble markers (sCD163, sCD14, soluble mannose receptor) show potential as disease biomarkers.
  • Advanced cytometry techniques enable comprehensive analysis of macrophage states.

Conclusions:

  • Macrophage plasticity is a central theme in disease pathogenesis and progression.
  • Targeting macrophage phenotypes offers promising therapeutic avenues, including TAM reprogramming and CAR-M cells.
  • Future research should focus on spatially resolved multi-omics, epigenetic/metabolic targeting, and standardized cytometry for personalized interventions.