Our immune system is an extraordinary sentinel that protects our body from harmful pathogens such us bacteria and viruses (the innate immunity), produce antibodies against foreign substances and destroy abnormal cells that may evolve into cancer cells (the adaptive immunity).

A balanced immune system can perfectly target and remove cancer cells before its evolution to a detectable tumour. However, an imbalanced immune system response could contribute to tumorigenesis or induce inflammation stimulating cancer cell proliferation and metastasis, leaving these cells growing effectively avoiding our immune system. Nowadays, we have acquired a strong understanding of how we can help our immune system play an effective role against cancer (or other diseases). It was in 2010 that the FDA approved the first immune therapy against prostate cancer, launching de facto the modern immunotherapy.

Cancer immunotherapy or immuno-oncology, by definition, represents a specific targeted therapy by using our immune system to fight and destroy cancer cells. As this does not involve surgery or use of radiation or chemotherapy, it is relatively safe to the healthy cells of the body. Importantly, it could be applicable at all stages of the disease, with higher efficiency.

The whole objective of Immunotherapy is to enable our immune system understand differences between healthy and cancer cells and then specifically target the cancer cells. We now have the tools to produce specific substances that stimulate our immune system to recognise and fight specific cancer cells. Monoclonal antibodies, checkpoint inhibitors and cytokines represent a class of immuno-oncology therapies that trigger an immune response to destroy cancer cells. As a fact, we have now several such therapies available to successfully treat several cancers including lung, kidney, bladder, head and neck, melanoma and some autoimmune diseases such as rheumatoid arthritis, psoriasis and alopecia.

In conclusion, immunotherapy (or immuno-oncology) has opened a new era in healthcare and indeed we can soon expect some ground-breaking discoveries that will completely erase our current notion of cancer as a life-threatening disease. Having said that, modelling the immune system in vitro to stimulate an effective response to cancer sets a particularly difficult challenge. Potential roles of multiple immune cells, the heterogeneity of tumours and the molecular mechanisms involved mean that multiple advanced assay models are required before moving the most promising immunotherapeutic approaches into clinical trials.

Cellomatics Biosciences Ltd. provides expertise in robust and reproducible Immuno-Oncology related assays. All assays can be customised to suit your requirements.


Antibody-dependent cellular cytotoxicity (ADCC), also referred to as antibody-dependent cell-mediated cytotoxicity, is a mechanism of cell-mediated immune defence whereby an effector cell of the immune system actively lyses a target cell, whose membrane-surface antigens have been bound by specific antibodies. It is one of the mechanisms through which antibodies, as part of the humoral immune response, can act to limit and contain infection.

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Antibody-dependent cellular cytotoxicity (ADCC)

Raji cells were treated with Anti-CD20 antibody and T cells and the Relative Luminescence Units (RLU) were measured 6 hours [A] and 24 hours [B] post incubation. The higher concentration of the Anti-CD20 resulted in an increase in the activation of the NFAT pathway. This corresponds directly to an increase in the target cell death.


Antibody-dependent cellular phagocytosis is the mechanism by which antibody-opsonized target cells activate the FcγRs on the surface of macrophages to induce phagocytosis, resulting in the internalization and degradation of the target cell through acidification of the phagosome.

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Antibody-Dependent Cellular Phagocytosis (ADCP)

The target Raji cells were pre-treated with or without Rituximab at different concentrations and stained with pHrodo Red (red). The THP-1 derived macrophages were stained with calcein (green). To assess antibody-dependent cellular phagocytosis of target Raji cells by THP-1 derived macrophages the two cell types were co-cultured for 6 hours. Data is represented as the red fluorescence intensity (RFI) at 0 hours vs. 6 hours in all treatment groups.

Immune Cell Killing

Natural killer cells and cytotoxic T lymphocytes (CTLs) perform complementary roles in immune responses directed against viruses and tumours. CTLs are antigen specific and recognize peptides derived from virus and tumour antigens presented by major histocompatibility complex (MHC) class I molecules. NK cells can recognize and kill cells that have down-regulated MHC class I molecules from their cell surface. The major cytotoxic proteins contained within secretory lysosomes in NK cells and CTLs are the granzymes and perforin. Target cell recognition induces secretory lysosome exocytosis and the release of the cytotoxic contents of this organelle. Perforin then facilitates the entry of the granzymes into the target cell cytoplasm, where they cleave a variety of targets, such as caspases, resulting in cell death (Topham and Hewitt, 2009).

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Immune cell killing

Quantification of Caspase 3/7 activity in a co-culture model of K562 cells incubated with unstimulated/stimulated primary CD56+ NK cells (**p<0.01; ***p<0.001; n=3 ± SEM). Staurosporine was used as a positive control.

PD-1/PD-L1 immune checkpoint Bioassay

The PD-1/PD-L1 Blockade Bioassay is a biologically relevant MOA-based assay that can be used to measure the potency and stability of antibodies and other biologics designed to block the PD-1/PD-L1 interaction.

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PD-1/PD-L1 immune checkpoint bioassay

The PD-1/PD-L1 luciferase bioassay enables detection of the inhibitory activity of anti-PD-1 and anti-PD-L1 blocking antibodies as quantified by increases in luminescence. In the assay workflow, PD-L1 expressing aAPC/CHO-K1 cells target cells are plated and treated with increasing concentrations of test antibodies along with the PD-1 expressing effector cells. Luminescence is detected after 6 hours using Bio-Glo™ Reagent and the GloMax® Discover System. Validation of the assay has been performed using Nivolumab and Pembrolizumab. EC50 for Nivolumab and Pembrolizumab is 0.28 µg/ml and 0.11 µg/ml respectively (a). The assay is specific for PD-1 blockade as confirmed by incubation with Ipilumamb, a CTLA-4 inhibitory antibody. A high degree of intra-plate reproducibility in Nivolumab inhibitory response is demonstrated (b).

PBMCs proliferate in response to anti-CD3 stimulation

PBMCs were treated for 96 hours with increasing concentrations of anti-CD3 antibody (0 µM, 0.25 µM, 1 µM and 5 µM; black bar) or with Isotype control (blue bar) or with Nivolumab (red bar). Supernatants were collected and IFN-γ release was quantified by ELISA. Results demonstrate a dose dependent increase in IFNγ levels which are further potentiated by PD-1 blockade as suggested by Nivolumab treatment.

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