The walls of your blood vessels are very good at keeping blood cells in. But to protect you from pathogens, white blood cells need to get out of the bloodstream and physically reach the infected organ.
So, how do they get out? By squeezing themselves out of little holes in blood vessel walls.
A research team led by Prof. Ronen Alon at the Weizmann Institute of Science studied this mechanism in more detail. They performed a series of experiments that looked at both the white blood cells, as well as the walls of the blood vessels (“endothelial cells”).
Previously, it was thought that white blood cells could get out because the blood vessel cells contracted like muscles in response to signals from the white blood cells. But, when Prof. Alon chemically disabled the blood vessel cells’ ability to contract in the lab, the white blood cells could still squeeze through just fine, disproving this hypothesis.
Instead, Dr Alon’s study found that the white blood cells deform the shape of their nuclei (this is the compartment of the cell that contains DNA) forming “nuclear lobes”, and push it to the front edge of their cells. This structure is able to bend the thin fibres that make up the scaffolding of the blood vessel (endothelial) cells. Small pores are generated, allowing the white blood cells to squeeze out of the blood vessel and reach the infected site. The pores are re-sealed by the endothelial cells as part of its routine maintenance.
A deeper understanding of the migration of immune cells could have important implications for future treatments. For instance, it is possible that a drug which slows down this process could help minimise harmful inflammation that occurs in autoimmune disorders. Alternatively, a different drug could speed up this migration process during infection, and could enable a speedier recovery.