Myeloid Cell Reprogramming and Immune Suppression

Abstract

Plasticity of myeloid cells, characterized by their ability to undergo reprogramming in response to environmental cues, is a fundamental feature enabling their versatile functions during immune responses. Macrophages and neutrophils, the primary myeloid cell types, exhibit distinct polarization states. Classical polarization states of macrophages and neutrophils are associated with antimicrobial activity, inflammation promotion, and tissue remodeling. Pathological polarization, observed in chronic inflammation, cancer, and other conditions, is marked by enhanced immune-suppressive activity, aberrant enzymatic activity, and atypical cytokine production, diverging from their classical functions. This review delves into the most up-to-date characterization of those polarization states, the transcriptional and epigenetic factors, and the metabolic pathways governing myeloid cell reprogramming, highlighting the influence of cytokines and tissue-specific conditions, such as hypoxia in tumors, on this process. Understanding the mechanisms underlying the pathological polarization of myeloid cells offers a promising avenue to modulate their activity for targeted therapeutic interventions.