Pro-inflammatory macrophage (M1 phenotype) (M1 macrophage)

M1 macrophages, or classically activated macrophages, are a pro-inflammatory phenotype of the myeloid lineage characterized by their ability to drive immune responses and directly eliminate pathogens or malignant cells (Frontiers in Oncology, 2019). In thyroid tissue, their role is highly dependent on the pathological state: they act as critical anti-tumor effectors in thyroid cancers, such as Papillary Thyroid Carcinoma (PTC), by producing reactive oxygen species and recruiting cytotoxic T cells, yet they are also primary drivers of follicular destruction in autoimmune diseases like Hashimoto's thyroiditis (Jaume et al., 2019; Frontiers in Immunology, 2020). These cells express specific markers such as CD80, CD86, and inducible nitric oxide synthase (iNOS), and secrete cytokines like TNF-α and IL-12 to maintain a pro-inflammatory environment (PMC, 2023). Therapeutic strategies in thyroid oncology frequently focus on "re-educating" tumor-associated macrophages (TAMs) from a pro-tumor M2 phenotype back to an anti-tumor M1 state using agents like CSF1R inhibitors, TLR agonists, and multi-kinase inhibitors (Naoum et al., 2018). Conversely, in Graves' disease or chronic thyroiditis, excessive M1 polarization is targeted for reduction to alleviate inflammation (B. fragilis Study, 2024). Because the entity "M1 macrophages in thyroid tissue" refers to a dynamic cell population rather than a specific molecule, it is typically modulated through receptors like GLP-1R or the TIM4/NLRP3 signaling axis (JCEM, 2024; PMC, 2021).

Other names

Classically activated macrophageKill-type macrophageM1-like tumor-associated macrophageM1-TAM

Induction of macrophage polarization from M2 (pro-tumor) to M1 (anti-tumor) phenotype via TLR4 activation or GLP-1R/PPARG/ACSL1 signaling; inhibition of CSF1R-mediated survival of immunosuppressive M2 macrophages; recruitment of cytotoxic T-lymphocytes through pro-inflammatory cytokine secretion.