Myeloid reprogramming in the tumour microenvironment
Myeloid reprogramming in the tumour microenvironment (TAMs & MDSCs). Tumours recruit and re-educate myeloid cells into immunosuppressive tumour-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs). CSF-1R and GM-CSF drive their survival and M2 polarisation; agonist anti-CD40 flips macrophages back to an anti-tumour M1 state. Click any protein for the matching Assay Genie In Vivo functional-grade antibody or ELISA kit.
Solid tumours secrete CSF-1 (M-CSF), GM-CSF and chemokines such as CCL2 (MCP-1) that recruit circulating monocytes and granulocytes and re-educate them. Signalling through CSF-1R (CD115) drives PI3K→AKT survival, ERK proliferation and STAT3/STAT6-dependent M2 polarisation, producing immunosuppressive tumour-associated macrophages (TAMs).
In parallel, myeloid-derived suppressor cells (MDSCs) — identified by CD11b with Ly6C (monocytic) or Ly6G (granulocytic) — accumulate and suppress T-cell responses. TAMs and MDSCs together dampen anti-tumour immunity, promote angiogenesis and support tumour growth. Agonist anti-CD40 signals through NF-κB to repolarise macrophages toward an inflammatory, anti-tumour M1 phenotype (IL-12, TNF-α).
Assay Genie In Vivo functional-grade antibodies address this compartment by blocking/depleting (anti-CSF-1R, anti-Ly6C, anti-Ly6G, anti-Gr-1), neutralising recruitment (anti-GM-CSF) and repolarising (agonist anti-CD40). For research use only; not for diagnostic or therapeutic procedures. Mouse targets shown.
Every protein node links to a product: surface / cytokine targets open Assay Genie In Vivo antibodies; signalling proteins open the matching ELISA kit.