Centre for Inflammation Research

Dr Clare Pridans

Clare’s research focuses on understanding the role of CSF1R signalling during macrophage development.

Dr Clare Pridans

Principal Investigator

  • Centre for Inflammation Research

Contact details

Group members

Alison Thomson - Postdoc


Macrophages are found in all mammalian tissues where they contribute to innate and acquired immunity, tissue development, homeostasis and repair; as well as the pathogenesis of inflammatory, neoplastic, and neurological diseases. Tissue-resident macrophages adapt to distinct tissue niches and environments to perform tissue-specific functions. Macrophage production and differentiation from bone marrow progenitor cells is controlled by macrophage colony stimulating factor (CSF1), which signals through the CSF1 receptor (CSF1R).

Research Overview

Current Projects

Identifying the role of microglia in mediating autism spectrum disorder (ASD)-relevant phenotypes in the developing and adult brain.

Clare recently published a mouse model in which a Csf1r enhancer (FIRE) was deleted using CRISPR/Cas9 (Rojo et al., Nature Communications 2019). Deletion of FIRE completely depleted macrophages in the skin, heart, kidney, peritoneal cavity, and the brain (microglia), yet the mice are healthy and fertile. The Csf1rΔFIRE/ΔFIRE mice are the first animal model to lack microglia that survive. Clare has funding from the Simon’s Initiative for the Developing Brain to investigate aspects of development known to be disrupted in models of ASD and for which microglia have been proposed to play a role. The work is performed in collaboration with Professors Giles Hardingham and Peter Kind at the University of Edinburgh.


Optimisation of novel CSF1R inhibitors – New drugs for osteoporosis.

Disruption of CSF1R signalling has therapeutic potential in inflammatory disease, cancer, autoimmunity and bone disease. For that reason, numerous companies have explored different options to block CSF1R signalling. When mice were treated with an anti-CSF1R antibody (Amgen. Inc), we found this prevented age-related osteoporosis in female C57BL/6 mice (Sauter et al., J Leukoc Biol. 2014). Another company, Plexxicon is currently using inhibitors in various cancer clinical trials. However, these inhibitors are not exclusively specific for CSF1R as they also target closely related kinases such as KIT. Eirik Sundby at the Norwegian University of Science and Technology has developed new CSF1R inhibitors that are more specific than the FDA-approved inhibitors used by Plexxicon. I have funding from the Norwegian Research Council to test these inhibitors in macrophage reporter rats (Csf1r-mApple) prior to use in a rat model of osteoporosis.


How do Csf1r mutations cause neurodegeneration and dementia?

Characterisation of a novel mouse model of human neurodegeneration.

Heterozygous mutations of CSF1R in humans causes the neurodegenerative disease adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP, previously known as HDLS). These mutations are loss-of-function (Pridans et al., Sci. Rep. 2013). Prior to the association with CSF1R mutations in 2011, ALSP was commonly misdiagnosed. Ante mortem diagnoses of autopsy-confirmed cases have included multiple sclerosis, frontotemporal dementia, Alzheimer’s disease and atypical Parkinson’s disease. The shared features suggest that ALSP may share pathogenesis with more common neurodegenerative diseases and may be more prevalent than is currently recognised. Clare has a new mouse model which contains one of the Csf1r mutations seen in humans (E631K). Preliminary analyses of the Csf1r+/E631K mice reveals a reduction in microglia as seen in ALSP patients. The Csf1rE631K/E631K mice fail to thrive, which is representative of infants with compound heterozygous or homozygous CSF1R mutations.  

An adult male CSF1R deficient rat
An adult male CSF1R deficient rat. Rats were created via homologous recombination in embryonic stem cells.



Analysis of rat macrophages.

Prior to genetic engineering in mice, rats were the research model of choice. Now that CRISPR/Cas9 technology is available, it is now possible to generate new rat models quite quickly. Many researchers, particularly in the area of neuroscience, are now favouring rats over mice. However, the basic studies of rat macrophages have not been performed. I am comparing gene expression of rat macrophages with those of mouse and human, including embryonic-derived macrophages. Utilizing microarray and RNA-seq data I will show that the response of rat macrophages to lipopolysaccharide (LPS) resembles the human response more than the mouse. 


Identifying the role of FIRE during embryonic microglia development using a novel Csf1r-reporter mouse.

The publication describing the Csf1rΔFIRE/ΔFIRE mice largely focused on the adult. We are now extending our analysis to embryos from E9 onwards, with an emphasis on microglia development. The Csf1rΔFIRE/ΔFIRE mice have been crossed with novel Csf1r-FusionRed reporters to enable macrophage visualisation. There are existing Csf1r-reporters that have been widely used – including the so-called ‘MacGreen’ mice. These mice were created 16 years ago via pronuclear injection of a plasmid containing the Csf1r promoter and FIRE enhancer upstream of GFP. The caveat with these mice is that there is GFP expression in cells which do not express CSF1R protein (B lymphocytes and neutrophils). The Csf1r-FusionRed mice were recently created via CRISPR/Cas9 which inserted the fluorescent protein sequence at the end of Csf1r. Unlike the MacGreen mice, I have shown that there is no transgene expression in non-myeloid cells (unpublished) and thus they are providing an excellent tool for my Csf1r research.

The following PDF provides a brief visual summary of this group’s current research.


You can view a full catalogue of graphical research summaries for each group in the Centre for Inflammation Research by visiting our Research page.

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Biographical Profile

Clare obtained her PhD in 2006 at the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia. Working with Professor Stephen Nutt, her work focused on the transcriptional regulation of B lymphocyte commitment. In 2007 Clare moved to the UK and spent 3 years working with Professor Brian Huntly at the Cambridge Institute for Medical Research. Here she investigated epigenetic signatures in human acute myeloid leukaemia. From 2010 to 2017 Clare worked with Professor David Hume at the Roslin Institute, University of Edinburgh. She will continue her research on CSF1R at the Medical Research Council Centre for Inflammation Research (CIR) at the University of Edinburgh from February 2018. 

Public Engagement

  • STEM Ambassador




  • Simon's Initiative for the Developing Brain
  • Norwegian Research Council

Information on funding at Clare Pridans' Research Explorer profile.