An international collaboration between Faculty scientists and the National Institutes of Health in America have discovered a new finding about how immune cells determine whether to repair or protect damage to the body.
The research, led by Dr John Grainger and Dr Yasmine Belkaid (National Institute of Allergy and Infectious Diseases, USA) will lead to improved treatments for a range of conditions from Inflammatory Bowel Disease (IBD) to cancers.
Their work specifically looked at specialised immune cells called monocytes. Monocytes, which are continuously being made in the bone marrow, are rapidly called to sites of injury in order to help the body heal. What makes monocytes so effective is their ability to change their function depending on the need of the body. For example, some can be used to repair and heal wounds, whilst others are used to protect the body from invading attackers.
However, in some situations, these monocytes choose the wrong function – choosing to protect when they should ‘attack’. This can have disastrous results, leading to disease like IBD and some types of cancer.
What’s been a puzzle for scientists is how these immune cells determine what action to take. Researchers assumed that the cells decide which function to fulfil when they arrive at the point of injury. Dr Grainger and his team used mouse models and the parasite Toxoplasma gondii to investigate how, and where, monocytes are programmed in response to toxoplasmosis.
Dr Grainger explains the results:
“Very soon after the toxoplasma invades the gut, the tissue starts to communicate with other parts of the body to alter the immune system. One particular cell-type in the gut, the dendritic cell, can act as a beacon sending out long-range signals to the bone marrow where monocytes are produced. Cells in the bone marrow then pick up the signal and pre-programme monocytes with the appropriate function to either protect or repair.”
This means that rather than waiting to get to the site of damage, monocytes are already programmed with a specific function.
This discovery could prove crucial because, based on the previous assumption, existing therapies focus only on the site of infection. This means a lot of therapies are reactive to the symptoms and do not treat the underlying cause. It is now thought that this research can help develop much more effective treatments which will help prevent inflammatory diseases before they start.
One final discovery the team made was that monocytes are able to change their behaviour from their pre-programmed state if they come across commensal (good) bacteria. Dr Grainger concludes:
“We were really blown away by the fact that the monocytes could change their function depending on the commensal bacteria in the gut. We’re all becoming increasingly aware of how different types of commensal bacteria can affect our health – what we need to do now is test whether specific species within the whole commensal group are responsible for influencing monocyte function in a particular way.”
The paper “Bone-Marrow-Resident NK Cells Prime Monocytes for Regulatory Function during Infection” will be published by the journal Immunity on Tuesday 9th June.