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Differentiation of Human induced Pluripotent Stem Cells to Authentic Macrophages using Defined, Serum Free, Open Source Media

ABSTRACT: Human iPSC and macrophages derived from them are increasingly popular tools for research into both infectious and degenerative diseases. However, as the field strives for greater modelling accuracy, it is becoming ever more challenging to justify the use of undefined and proprietary media for the culture of these cells. We describe here a defined, serum-free, open-source medium for the differentiation of iPSC-derived macrophages. This medium is equally capable of maintaining these cells compared to commercial alternatives. The macrophages differentiated in this medium display improved terminally differentiated cell characteristics, reduced basal expression of induced anti-viral response genes, and improved polarisation capacity. We conclude that cells cultured in this medium are an appropriate and malleable model for tissue resident macrophages, on which future differentiation techniques can be built.

ORGANISM(S): Homo sapiens

PROVIDER: GSE171313 | GEO | 2021/04/02

REPOSITORIES: GEO

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Project description:This mathematical model of the role of the innate immune responses generated by macrophages in the context of anti-tumour oncolytic viral therapies is described in the publication: Nada Almuallem, Dumitru Trucu, Raluca Eftimie. "Oncolytic viral therapies and the delicate balance between virus-macrophage-tumour interactions: A mathematical approach". Mathematical Biosciences and Engineering, 2021, 18(1): 764-799. doi: 10.3934/mbe.2021041 Comment: This model is represented by Equations 2.1a-f of the publication manuscript. Abstract: The success of oncolytic virotherapies depends on the tumour microenvironment, which contains a large number of infiltrating immune cells. In this theoretical study, we derive an ODE model to investigate the interactions between breast cancer tumour cells, an oncolytic virus (Vesicular Stomatitis Virus), and tumour-infiltrating macrophages with different phenotypes which can impact the dynamics of oncolytic viruses. The complexity of the model requires a combined analytical-numerical approach to understand the transient and asymptotic dynamics of this model. We use this model to propose new biological hypotheses regarding the impact on tumour elimination/relapse/persistence of: (i) different macrophage polarisation/re-polarisation rates; (ii) different infection rates of macrophages and tumour cells with the oncolytic virus; (iii) different viral burst sizes for macrophages and tumour cells. We show that increasing the rate at which the oncolytic virus infects the tumour cells can delay tumour relapse and even eliminate tumour. Increasing the rate at which the oncolytic virus particles infect the macrophages can trigger transitions between steady-state dynamics and oscillatory dynamics, but it does not lead to tumour elimination unless the tumour infection rate is also very large. Moreover, we confirm numerically that a large tumour-induced M1→M2 polarisation leads to fast tumour growth and fast relapse (if the tumour was reduced before by a strong anti-tumour immune and viral response). The increase in viral-induced M2→M1 re-polarisation reduces temporarily the tumour size, but does not lead to tumour elimination. Finally, we show numerically that the tumour size is more sensitive to the production of viruses by the infected macrophages.

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Differentiation of Human induced Pluripotent Stem Cells to Authentic Macrophages using Defined, Serum Free, Open Source Media

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