Tabular representation of various oncogenic cells at TME

Tumor microenvironmentDifferent cells at TMENatureInferenceReference
Cancer and cancer associated cells at TMECancer cellsProtumorCancer cells contribute to metabolic reprogramming of other cancer associated cells and immune cells thus supporting tumorigenesis at TME.[10]
TSAsProtumorTSAs meets the energy demand presented before them by cancer cells for pivotal oncogenic regulation at TME. This is marked with amplified pro-inflammatory expression of cytokines (IL-1β, IL-6, IL-10), MMP-11 etc.[11]
TSECsProtumorTumor specific endothelial cells (TSECs) has their decisive role in tumor metastasis, where angiogenesis, vascular permeability, transport regulation etc. redirect immune cells and other cells at TME.[12, 13]
TSPsProtumorTSPs has crucial role in angiogenic regulation (blood vasculature, extracellular matrix remodeling) at TME.[10]
TSFsProtumorRole of TSFs in oncogenic invasion, proliferation and angiogenesis. Its crosstalk with resident immune cells reveals that secretion (TGF-β, IL-10, M-CSF) from TSFs target antitumor immune cells either by restraining their response generation or by dysfunctional response initiation (T cells, NK cells, DCs etc.), while differentiating other immune cells (TAM2, TAN2, Treg etc.) to acquire protumor phenotype with tumor supporting action.[14]
Immune cells at TMETANsTAN2
TAN1		Presence of TAN2 type neutrophils recruits other protumor immune cells performing tumorigenic activities such as angiogenesis and metastasis by release of VEGF, ROS, inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-12) etc.[17]
TAMsTAM1
TAM2		Crosstalk with other immune cells (MDSCs, Treg, Th2, CD8+ cells, NK cells etc.) cancer cells and cancer associated cells contributes to oncogenic regulations leaded by release of VEGF, cytokines (IL-1, TNF-α), extracellular matrix (ECM) degrading molecules [urokinase-type plasminogen activator (uPA), MMP7, MMP9 etc.] further additional factors such as TGF-β, HGF/basic fibroblast growth factor (bFGF)/prostaglandin E2 (PGE2) etc. are also involved in immune suppressive action.[18, 19]
MDSCsProtumorMDSCs interact with both residing tumor and immune cells and initiate a signaling event where it amplifies immune suppressive expression.[20]
TregsProtumorIt targets functional activity of T cells, NK cells in indirect and direct way.[21]
DCsProtumor tDCs
Antitumor DCs		tDCs represent inferior level of costimulatory molecules (CD80, CD86) expressed on their surface, vice-verse reported for inhibitory molecules (PD-L1/CTLA-4 etc.) responsible for immune suppressive action. The stimuli input for tDCs functioning comes from VEGF/cytokines (TGF-β, IL-10), and IL-10 secreting Treg cells etc. they liberate a range of immunomodulatory factors (TRAIL/PD-L1/DC-SIGN galactin-1) and immunosuppressive molecules (TGF-β/IL-10/IL-27/NO/IDO).[22, 23]
CTLsAntitumorObstacle at Th1 mediated antitumor immunity promote protumor immune response.[23]
NK cellsAntitumorRelease of TGF-β, IFN-γ, STAT3, hypoxia like factors downregulates NK cells active expression.[24]