An interview with Elodie Segura on ‘TLR or NOD receptor signaling skews monocyte fate decision via distinct mechanisms driven by mTOR and miR-155’

This content is part of the Research in Practice in Immunology series of interviews with scientists, focusing on how their research work can have impact on medical practice. Click here to follow 'Research in Practice in Immunology' - for free - on Researcher for more great interviews.

Could you tell us about who you are, where you work and what you're currently working on?

My name is Elodie Segura. I'm a researcher at the National Institute for Health and Medical Research in France, INSERM and more specifically, I work at the Institute Curie, Paris. The focus of our research is to understand how some groups of immune cells called mononuclear phagocytes, adapt their transcriptional and functional response to signals, from their microenvironment.

Could you tell us about your paper and why this topic is so important?

In this paper, we are focusing on this population called monocytes, which are present in the blood, and they circulate until they are called into tissues by inflammation, for instance, when there is an injury or infection. This is interesting to us because when they exit the blood, they differentiate into other cell types. They can differentiate into macrophages, which are specialised in taking up debris, dead cells and pathogens and inducing tissue repair or into dendritic cells, which have a completely different function and are specialised in presenting antigens to other cells of the immune system and activating an adaptive immune response. We wanted to understand how the monocytes decide to become one or the other. In this paper, we focused on a particular question, which is whether the recognition of pathogens can influence this process of fate’s decision.

Why is this topic important? It's because the monocytes have been shown to be deleterious in chronic inflammatory diseases, such as Crohn's disease, rheumatoid arthritis, multiple sclerosis or even cancer. When there is too much differentiation into macrophages, for instance, in cancer, then it will inhibit immune responses. On the other hand, when there is too much differentiation into dendritic cells, like in chronic inflammatory diseases, there will be too much activation of the inflammatory cascade leading to pathology. If we better understand how the monocytes decide to become one or the other side, and the molecule regulators of this process, we can opt to manipulate this for therapeutic purposes.

What's the connection between your research and medical practice? How do you hope that your work will have an impact on therapies or treatments in the future? 

We work on very fundamental and basic scientific questions in our lab, we hope that our research and our findings can be used for designing new therapeutic strategies. For instance, if we find some molecular regulators of monocytes fade decision, then we can manipulate these for therapeutic purposes. In cancer, we want to prevent the monocytes to differentiate into macrophages. If we find a way to block this, then we can opt to improve therapies for cancer patients. On the other end, for instance, in rheumatoid arthritis or multiple sclerosis, if we can lock the differentiation of monocytes into dendritic cells, using pharmacological inhibitors, then we hope to stop the inflammation vicious circle, and then improve the treatment of these patients. That's a long-term goal for us but we believe that our work should lead to some new discoveries that can lead to the identification of new molecular targets.

Where could your work lead you next and what's the dream outcome here for you?

The ultimate goal would be to identify druggable targets that can be easy to inhibit using medication for patients and that could be useful in several inflammatory diseases.

You can read and discover Elodie Segura’s research here.

TLR or NOD receptor signaling skews monocyte fate decision via distinct mechanisms driven by mTOR and miR-155 is published in PNAS

Photo Credits: Loop 

Disclaimer: This is a transcript of a video conversation. You can listen to the recording on Researcher.