Apoptosis and macrophages
Dying cells interfere with immune response
Immune cells give priority to cleaning from cells in a state of apoptosis, which prevents their normal migration to the sites of damage, according to the University of Sheffield website: Dead cells disrupt how immune cells respond to wounds and patrol for infection. Article by Roddie et al. Simu-dependent clearance of dying cells regulates macrophage function and inflammation resolution published in the journal PLOS Biology.
A study conducted by scientists from the University of Sheffield has shown that cells programmed to die (a process known as apoptosis) can disrupt the normal function of immune cells called macrophages. This can affect how well they respond to wounds and detect infections in the body.
Macrophages are essential at wound sites to prevent infection and aid healing processes, but at the same time, these cells can cause and worsen many human diseases, including cancer, heart disease and neurodegenerative disorders.
The study, which aims to understand how immune cells are controlled, can help create new treatments and accelerate healing processes. This work gives scientists a new understanding of the mechanisms that control immune cells in our body: for example, how they get to injury sites and stay in them.
Dr Ivan Evans, from the Department of Infections, Immunity and Cardiovascular Diseases at the University of Sheffield, who co-authored the paper, said: "Billions of cells die in our body every day, and many of them are removed and digested by our immune cells. If the removal process goes wrong, it can lead to autoimmune conditions. Excessive or inadequate immune responses worsen or cause a very wide range of human diseases from cancer to neurodegeneration. This work studies the fundamental biological processes that occur inside our body every day and that are necessary to maintain our health."
Studies on the interaction between dying cells and immune cells have been conducted using fruit flies, which contain macrophage-like cells very similar to our own immune cells. The new study also uncovered a new role for a protein called Six-Microns-Under (or Simu) in preserving immune cells at injury sites. Without this protein, macrophages prematurely left the wound sites.
Hannah Roddy – co-author of the study and a researcher in the Department of Infections, Immunity and Cardiovascular Diseases at the University of Sheffield – said: "The study shows that the way fruit fly blood cells respond to injury and dying cells is even more similar to how our own immune cells react than previously thought. Now we are studying what signals macrophages use to track dying cells and how they choose between dead cells and wounds. We understand with interest how immune cells are preserved at the sites of damage."
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