Tumor
Microenvironment
ELISA
Quantitative ELISA kits spanning the full TME — cytotoxic effectors, MDSC-driven suppression, TAM polarisation, Treg mediators, pro-inflammatory cytokines, and co-stimulatory TNF-R targets. Human, Mouse, and Rat validated. ISO 13485 manufactured. 14+ species for select cytokines.
Browse Assay Table → TME BiologyThe Tumor Microenvironment — A Balance of Forces
The tumor microenvironment (TME) is the ecosystem surrounding tumour cells — comprising immune cells, stromal cells, blood vessels, and the extracellular matrix, all communicating through a dense network of soluble mediators. Whether a tumour grows unchecked or is destroyed by the immune system depends on the balance between pro-inflammatory, cytotoxic forces and immunosuppressive, tumour-promoting ones. Quantitative ELISA of soluble TME factors in tumour-conditioned media, serum, plasma, ascites, and BAL fluid reveals the functional state of this balance — and how it shifts with therapy.
Anti-tumour Pro-tumour / Immunosuppressive
Perforin ↑ — Pore-forming lytic molecule
IFN-γ ↑ — MHC-I upregulation • Tumour immunogenicity
TNF-α ↑ — Direct tumour killing • ADCC
IL-12 ↑ — Th1 polarisation • NK activation
OX40 / 4-1BB ↑ — T cell survival & memory
IL-10 ↑ — M2 TAM • Treg expansion • CTL blunting
TGF-β1 ↑ — Fibrosis • Treg induction • CTL exclusion
STAT3 ↑ — IL-6 signalling • Immune evasion
VEGF ↑ — Immunosuppressive angiogenesis
IL-6 ↑ — Treg/Th17 imbalance • MDSC recruitment
| Cell Type | Function in TME | Key ELISA Markers | Research Context |
|---|---|---|---|
| CD8+ CTL | Tumour lysis, IFN-γ secretion | Granzyme B • Perforin • IFN-γ | Checkpoint therapy efficacy, CAR-T monitoring |
| NK Cells | MHC-I-independent killing, ADCC | Granzyme B • Perforin • IFN-γ | NK cell therapy, bispecific Ab CRS monitoring |
| MDSCs | T cell suppression, VEGF secretion | Arginase-1 • IL-10 • VEGF • STAT3 | Therapy resistance, MDSC-targeting studies |
| M2 TAMs | Tumour promotion, angiogenesis | IL-10 • TGF-β1 • Arginase-1 • MCP-1 | TAM repolarisation, CSF1R inhibitor studies |
| Tregs | Immune suppression, CTLA-4+ | IL-10 • TGF-β1 | Anti-CTLA-4 therapy, Treg depletion |
| M1 TAMs / DCs | Antigen presentation, IL-12 secretion | TNF-α • IFN-γ • IL-12 • CD40 | CD40 agonist studies, DC vaccination |
| Tumour cells | Cytokine secretion, MDSC recruitment | IL-6 • IL-8 • MCP-1 • VEGF • STAT3 | Resistance mechanisms, TME profiling |
Cytotoxic Effector ELISA
Granzyme B, Perforin, and IFN-γ are the three primary readouts of CTL and NK cell anti-tumour activity in the TME. Together they confirm that cytotoxic immune cells are not only present but functionally active — a distinction that tumour-infiltrating lymphocyte (TIL) counts alone cannot provide. Essential for evaluating checkpoint inhibitor efficacy, CAR-T function, NK cell therapy, and bispecific antibody T cell engagement.
Granzyme B is a serine protease stored in cytotoxic granules of CD8+ T cells and NK cells. It is released into the immunological synapse upon target cell recognition, enters the target cell via Perforin-formed pores, and activates caspase-dependent apoptosis. Elevated circulating Granzyme B is a validated pharmacodynamic marker of checkpoint inhibitor efficacy and correlates with response to pembrolizumab, nivolumab, and atezolizumab in NSCLC and melanoma. Also the primary pharmacodynamic readout for CAR-T and BiTE therapies.
Perforin is a pore-forming protein co-released with Granzyme B from cytotoxic granules. Perforin polymerises in the target cell membrane to create transmembrane pores through which Granzymes enter — without Perforin, Granzyme B-mediated killing cannot occur. Serum Perforin is measurable during active cytotoxic immune responses and serves as a complementary readout to Granzyme B. Particularly relevant in NK cell function studies, haemophagocytic lymphohistiocytosis (HLH) research, and monitoring of lymphocyte-mediated toxicity in immunotherapy.
Interferon-gamma is secreted by activated CD8+ T cells, NK cells, and Th1 CD4+ T cells. In the TME it drives MHC-I and MHC-II upregulation on tumour cells, increasing immunogenic visibility. IFN-γ also induces PD-L1 expression on tumour cells — a key mechanism by which immune activation paradoxically activates immune checkpoints. IFN-γ response signatures are used as predictive biomarkers for checkpoint inhibitor response and are required readouts in IO combination studies. Available in 14+ species.
MDSC, TAM & Treg Suppression Markers
MDSCs, M2-polarised TAMs, and Tregs are the dominant immunosuppressive populations in most solid tumours. They share several key soluble mediators — measuring these in tumour-conditioned media, ascites, or patient serum reveals the immunosuppressive burden of the TME and identifies candidates for combination IO therapy.
Arginase-1 is the primary effector enzyme of MDSC-mediated immunosuppression. MDSCs and M2-polarised TAMs secrete high levels of Arginase-1 into the TME, depleting local L-arginine — an amino acid required for T cell receptor zeta-chain expression and TCR signalling. L-arginine depletion causes reversible T cell anergy without killing them. This is one of the most targetable MDSC suppression mechanisms: Arginase inhibitors (e.g. INCB001158) are in clinical trials in combination with pembrolizumab. Serum Arginase-1 also correlates with MDSC abundance and tumour burden in solid tumours. Available in Human, Mouse, and Rat.
STAT3 is a transcription factor activated downstream of IL-6, IL-10, and oncogenic receptor tyrosine kinases. In the TME, constitutive STAT3 activation in tumour cells and immune cells drives immune evasion by upregulating immunosuppressive cytokines (IL-10, VEGF, IL-6), downregulating MHC-I expression, and promoting MDSC expansion and survival. STAT3 is also a key mediator of cetuximab resistance in EGFR+ colorectal cancer and of castration resistance in prostate cancer via IL-6 signalling. Soluble STAT3 in serum is an emerging biomarker for disease aggressiveness across multiple tumour types.
IL-10 is a pleiotropic anti-inflammatory cytokine secreted by M2-polarised TAMs, Tregs, MDSCs, and some tumour cells. In the TME, IL-10 suppresses M1 macrophage activation, reduces MHC-II expression on APCs, inhibits Th1 cytokine production, and promotes Treg expansion — collectively blunting CD8+ T cell-mediated anti-tumour immunity. Elevated serum or ascites IL-10 correlates with poor prognosis in ovarian, gastric, and non-Hodgkin's lymphoma. Measuring IL-10 alongside IFN-γ provides the Th1/Treg balance readout central to many IO studies. Available in Human, Mouse, and Rat.
TGF-β1 is a master immunosuppressive and fibrogenic cytokine in the TME. It drives Treg induction from naïve CD4+ T cells, excludes effector T cells from the tumour core by promoting fibrotic stroma, suppresses NK cell cytotoxicity, and promotes epithelial-to-mesenchymal transition (EMT). TGF-β signalling is a major mechanism of resistance to anti-PD-1/PD-L1 therapy — particularly in "immune-excluded" tumours where T cells accumulate in the stroma but cannot penetrate the tumour nest. TGF-β-blocking strategies in combination with checkpoint inhibitors are in active clinical development for multiple tumour types. Available in Human, Mouse, and Rat.
TME Cytokine & Chemokine ELISA
Pro-inflammatory cytokines in the TME have paradoxical roles — they can drive anti-tumour immunity when produced by CTLs and M1 macrophages, but promote tumour progression and therapy resistance when produced chronically by tumour cells or stromal fibroblasts. Quantitative ELISA in conditioned media, serum, and tissue lysates distinguishes these contexts.
IL-6 activates STAT3 in tumour cells and immune cells, promoting survival, proliferation, and immune evasion. In the TME, IL-6 drives MDSC recruitment and M2 TAM polarisation. It is also the primary driver of cytokine release syndrome (CRS) in CD3-bispecific and CAR-T therapy — making it an essential safety biomarker. Tocilizumab (anti-IL-6R) is standard of care for CRS management. Available in Human, Mouse, Rat, and 6+ additional species.
TNF-α has dual roles in the TME — at high concentrations it mediates direct tumour cell killing via TNFR1 (apoptosis) and potentiates ADCC by NK cells. At low chronic concentrations it promotes tumour survival and EMT via NF-κB activation. TNF-α is a key readout for macrophage and DC activation, and a pharmacodynamic marker for immune activation in checkpoint therapy. Available in Human, Mouse, Rat, and 10+ additional species including NHP and canine.
IL-8 (CXCL8) is secreted by tumour cells, TAMs, and stromal fibroblasts in the TME, where it recruits tumour-associated neutrophils (TANs) and MDSCs via CXCR1/CXCR2 signalling. Elevated serum IL-8 is a negative predictive biomarker for anti-PD-1 therapy response — patients with high baseline IL-8 respond poorly to pembrolizumab and nivolumab. IL-8 also promotes angiogenesis and tumour invasion. It is routinely measured in TME profiling studies alongside VEGF, IFN-γ, and IL-6.
MCP-1 (CCL2) is the primary chemokine responsible for recruiting monocytes and macrophages from the bloodstream into the tumour, where they differentiate into TAMs. High tumour MCP-1 expression correlates with high TAM infiltration and poor prognosis in breast, prostate, and colorectal cancer. Several CCR2 inhibitors are in clinical development to reduce TAM recruitment and improve checkpoint inhibitor response. MCP-1 is also relevant in ascites TME characterisation in ovarian cancer. Available in Human, Mouse, and Rat.
IL-1β is processed and secreted via the NLRP3 inflammasome in TAMs and MDSCs, promoting tumour cell survival, invasion, and angiogenesis via NF-κB and COX-2 induction. Elevated TME IL-1β correlates with metastatic disease in breast, lung, and CRC. IL-1β also drives the MDSC-promoting microenvironment in the bone marrow in multiple myeloma. Canakinumab (anti-IL-1β, approved for systemic JIA) has shown promising signals in reducing lung cancer incidence in the CANTOS trial.
IL-4 (KBH8011) drives M2 macrophage polarisation and Th2 skewing in the TME, contributing to the immunosuppressive microenvironment. Elevated in some breast and pancreatic cancers. IL-21 (KBH0057) is secreted by T follicular helper cells and NK cells; it promotes B cell differentiation and enhances CD8+ CTL cytotoxicity and NK cell killing — making it a potential immunostimulatory cytokine in IO. Both available in Human and Mouse.
TNF-R Superfamily Agonist Targets
The TNF-R superfamily includes several co-stimulatory receptors on T cells and NK cells that amplify immune activation when engaged — in contrast to checkpoint receptors, which suppress it. Agonist antibodies targeting these receptors are in active clinical development as IO combination agents. Soluble forms are measurable in serum and serve as pharmacodynamic readouts for agonist antibody engagement.
OX40 (CD134) is expressed on activated CD4+ and CD8+ T cells and Tregs. OX40 agonist antibodies promote T cell expansion, effector function, and memory formation while depleting immunosuppressive Tregs within the tumour. Available in Human, Mouse, and Rat.
CD137 (4-1BB) is induced on CD8+ T cells and NK cells post-activation. Agonist antibodies (utomilumab, urelumab) enhance CTL survival, cytokine secretion, and cytotoxic activity. Available in Human and Mouse.
GITR is upregulated on tumour-infiltrating Tregs and effector T cells. Anti-GITR agonists promote effector T cell activation while depleting intratumoral Tregs. Available in Human.
CD40 expressed on DCs, macrophages, and B cells. CD40 agonists activate APCs, inducing IL-12 secretion and enhancing cross-presentation — particularly relevant in immunologically "cold" tumours like PDAC. Available in 6 species including Human, Mouse, and Rat.
BAFF (B cell-activating factor) is a TNF-family cytokine critical for B cell survival and differentiation. In the TME, BAFF is produced by TAMs and tumour cells and supports tumour-infiltrating B cell populations (TIBs) and plasma cells. Elevated in B cell malignancies and relevant in CAR-B research. Available in Human, Mouse, and Rat.
HVEM (Herpesvirus Entry Mediator) has dual functions — it delivers co-stimulatory signals via LIGHT/LTα and inhibitory signals via BTLA and CD160. HVEM expression on T cells and tumour cells creates a complex bidirectional signalling network that can either stimulate or suppress depending on ligand context. Relevant in melanoma, CLL, and DLBCL TME research. Available in Human.
TME ELISA — Full Table
Contact info@krishgen.com for pricing, validation data, and multi-species availability confirmation.
| Category | Target | TME Role | Species | Cat No. |
|---|---|---|---|---|
| Effector | Granzyme B | CTL / NK cytotoxic activity • Checkpoint PD marker | Hu • Mo • Ra | KBH0899 |
| Effector | Perforin | Pore-forming lysis • NK cell function | Hu • Mo • Ra | KBH7989 |
| Effector | IFN-γ | MHC-I induction • Th1 • PD-L1 driver | 14+ species | KB1053 |
| Suppress | Arginase-1 ARG1 | MDSC • L-arginine depletion • T cell anergy | Hu • Mo • Ra | KBH4984 |
| Suppress | STAT3 | IL-6/JAK2 • Immune evasion • Drug resistance | Hu • Porcine | KBH0650 |
| Suppress | IL-10 | M2 TAM • Treg • APC suppression | Hu • Mo • Ra | KBH8021 |
| Suppress | TGF-β1 | Treg induction • T cell exclusion • Fibrosis | Hu • Mo • Ra | Contact us |
| Cytokine | IL-6 | STAT3 • MDSC recruitment • CRS marker | 8+ species | KBH8009 |
| Cytokine | TNF-α | Tumour killing • ADCC • NF-κB | 10+ species | KB1145 |
| Cytokine | IL-8 / CXCL8 | MDSC / TAN recruitment • PD-1 resistance | Human | KB1070 |
| Cytokine | MCP-1 / CCL2 | Monocyte / TAM recruitment • Ascites | Hu • Mo • Ra | KB1094 |
| Cytokine | IL-1β | NLRP3 inflammasome • NF-κB • Angiogenesis | Hu • Mo • Ra | KBH8054 |
| Cytokine | IL-4 | M2 polarisation • Th2 skewing | Hu • Mo | KBH8011 |
| Cytokine | IL-21 | CTL / NK enhancement • TFH marker | Hu • Mo | KBH0057 |
| Cytokine | IL-12/IL-23 p40 | Th1 polarisation • M1 macrophage • DC activation | Hu • Mo • Ra | KBH8019 |
| Cytokine | IL-2R / CD122 | T cell activation marker • IL-2 pathway | Human | KBH0315 |
| Co-stim | OX40 / CD134 | T cell survival / memory • Treg depletion | Hu • Mo • Ra | KBH3356 |
| Co-stim | 4-1BB / CD137 | CD8+ T / NK activation • Agonist target | Hu • Mo | KBH6343 |
| Co-stim | GITR (TNFRSF18) | Treg depletion • Effector T cell activation | Human | KBH6339 |
| Co-stim | CD40 (TNFRSF5) | DC / APC activation • Cold tumour immunisation | 6 species | KBH11145 |
| Co-stim | BAFF (TNFSF13B) | B cell / TIB survival • B cell malignancies | Hu • Mo • Ra | KBH1967 |
| Co-stim | HVEM (TNFRSF14) | BTLA / CD160 axis • Dual co-stim / inhibitory | Human | KBH6641 |
EffectorAnti-tumour cytotoxic markers SuppressImmunosuppressive mediators CytokinePro-inflammatory TME cytokines Co-stimTNF-R co-stimulatory receptors
Common Questions — TME ELISA
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