CCL2 and neoplasm: For example, they can be used to inhibit CD47, an antiphagocytic ligand exposed by tumor cells to evade immune system recognition; to block macrophage receptors for “do not eat me” ligands including the signal regulatory protein-a (SIRP-a), leukocyte immunoglobulin-like receptor B 1/2 (LILRB1/2) and Sialic acid-binding Ig-like lectin 10 (SIGLEC10); to activate the T cell by joining to CD3, CD28 or 4-1BB and promoting T cell proliferation and function; and, to block soluble factors such as CCL2, CLL5, CXCL12, CSF-1 and VEGF-A given off by tumor cells to create an immunosuppressive TME [90].