How sleep can boost your body's immune response
Researchers have demonstrated the importance of good-quality sleep time and time again, showing that a solid night’s rest can contribute to many aspects of physical and mental well-being. One new study has explained how sleep contributes to the proper functioning of the immune system.
Getting enough good-quality sleep each night is essential if we want to stay healthy and function well throughout the day.
Studies have shown that being sleep deprived is akin to overdrinking when it comes to its effects on the brain.
Recent research also suggests that poor sleep increases pain sensitivity and may raise the likelihood of developing cardiovascular problems.
Now, a study recently conducted by a team from the University of Tübingen in Germany has found a mechanism linking sleep to the functioning of the immune system.
The researchers who led this study found that a good night’s sleep can boost the effectiveness of certain specialized immune cells called T cells.
In the study paper — which now appears in the Journal of Experimental Medicine — the scientists explain what lies at the core of this relationship between sleep and the body’s defenses against infection.
T cells contribute to the body’s immune response when a potentially harmful foreign body enters the system.
These immune cells recognize pathogens then activate integrins, which are a type of protein that allows T cells to attach to and tackle their targets.
The researchers note that little is known about how T cells activate integrins, as well as what may prevent these cells from attaching to potentially compromised targets.
To learn more about these mechanisms, the team focused on Gs alpha-coupled receptor agonists (Gas-coupled receptor agonists). These are signaling molecules, many of which have the ability to block the action of the immune system.
Through laboratory analyses, they found some Gas-coupled receptor agonists that stopped T cells from activating integrins, thus preventing them from attaching to their targets.
The receptor agonists they found included two hormones (called adrenaline and noradrenaline), two proinflammatory molecules (called prostaglandin E2 and D2), and adenosine (which is a chemical that plays a key role in cellular signaling and energy transfer).
“The levels of these molecules needed to inhibit integrin activation,” says study co-author Stoyan Dimitrov, “are observed in many pathological conditions, such as tumor growth, malaria infection, hypoxia, and stress.”
He goes on, “This pathway may therefore contribute to the immune suppression associated with these pathologies.”