• Consultants in designing a model for immune response study in vitro and in vivo
  • Laboratory experiments (in vitro and/or in vivo) to test a model
  • Human in vitro systems

Immune modelling is the designing of an experimental model to test the immune response that may be associated with an infection, a metabolite or a drug. In immuno oncology it would be the key source to understanding the effective pathway of a therapeutic for example an oncolytic agent.

This is most appropriate when you are looking for a customised solution to a problem that cannot be solved by a single or standard assays. We work very closely with our clients to understand and troubleshoot problems they might have had with previous preclinical experiments (in vivo or in vitro), or to design a suitable experimental model to study the immunobiology associated with their product. Depending on the mechanism of the drug and the target tissue the experimental model can involve a number of customised immune assays such as dendritic cell assay, T cell assay, immune checkpoint assays, mixed lymphocyte (MLR) assay, tissue damage assay,cytokine release assay, ADCP, phagocytosis, macrophage assays, immune functional assays, M1/M2 macrophage polarisation assay, Th1/Th2/Th17 differentiation assays, etc. These assays can be performed with PBMCs and with human cell lines.





An immune model is very useful if developing or testing an immunotherapeutic that is expected to function through generating an immune response (e.g. against tumours) or if the drug targets an immune condition (e.g. autoimmunity) or if the drug might generate an adverse immune response. This can also be combined with a mathematical model.

The adaptive immune system is a very complex system that is structured through a cascade of cells, receptors and cytokines that process, respond, initiate, memorise and deliver an immune response or tolerance. Understanding the threshold of ‘TOLERANCE’ is important to determine the mechanism of a therapeutic that exerts its effect through an immune response or that is likely to cross paths with the immune system.

In a sterile inflammatory state, as in a drug-induced effect, the immune effectors interact with the tissue of the body and/or the therapeutic agent to produce a cell mediated and/or antibody mediated immunity.

We have the relevant experience and insight to help you study the IMMUNE RESPONSE through the appropriate immune model and disease model.

Relevant to your work if you are:

  • Working in immuno oncology, e.g. generating an immune response against an oncolytic virus or other form of tumour targeted antigen carrier
  • Working in vaccine development against an infection or autoimmune disease
  • Working in autoimmune disease
  • Developing a large molecule therapeutic that requires more understanding of associated protein signaling pathways
  • Developing a therapeutic (small or large molecule) that could interact with a non-target tissue.


We will first learn from you the mode of action of the therapeutic and the target tissue. From our team of protein and immunology experts, we will then design an experimental model for in vivo and/or in vitro (human) to test the immune response in the relevant disease model. The laboratory experiments will be carried out through an array of assays within our capacity.

Every study is tailored to the need of the therapeutic in reference, hence maybe different in timeline, process and pricing.


To study the role of heat shock proteins in immune mediated cell death and autoimmunity a model of diabetes was designed that consisted of transgenic expression of the target protein. Cell death of islet beta cells was initiated in a controlled dose dependent manner. The study successfully revealed that the (i) the initial beta cell death was responsible for the initiation of an immune mediated diabetes, and (ii) the immune response was increased by the over expression of heat shock protein. This study was important to understand the role of heat shock proteins in immunogenicity following tissue damage.

Dose dependent controlled death of islet beta cells was induced to initiate peptide targetted autoimmune response. The role of Heat shock protein in immune mediated cell death was studied. The overexpression of Heat shock protein (panel B) caused increased cell death as evidenced by reduction in insulin production on day 21 (diabetes development).

This also correlated with diabetes measurement (A = control, B = overexpression of Heat shock protein)

The death of beta cells and development of diabetes due to heat shock protein expression association was an immune mediated process.

Immunhistochemistry showed increased infiltrations (panel B) of MHC ClassII positive cells in the pancreas and inflammatory cytokines such as IL-1beta were elevated in serum.