PhotoScientists have constantly been striving to understand how and why our immune systems break down as we get older. While certain studies have shown promise in boosting immune systems for the elderly, the exact mechanism that degrades our ability to fight infection and disease has remained somewhat unknown.

That is, until now. Researchers at Oxford University and Basel University have found which genes are affected by a certain protein called Foxn1, which is largely responsible for regulating our immune systems. Declining levels of this protein inhibits production of T cells, which are essential in order for us to remain healthy.  

Understanding immunity

Researchers have found that declining levels of Foxn1 led to a sort of chain reaction when it came to the degradation of our immune systems. Everything related to this crucial system starts in the thymus, an organ where T cells are created.

As T cells develop in the thymus, they interact with thymic epithelial cells (TEC). This is a necessary interaction, since scientists have found that people without TEC are unable to produce functioning T cells; and without T cells, the immune system is severely compromised.

This is where Foxn1 comes into play; this protein is directly responsible for creating TEC in the thymus. Lowered levels of Foxn1 prevent TEC from being created, but until now researchers weren’t sure which genetic factors were controlled by Foxn1 that made this the case.

Using a range of models and analytical tools, scientists were able to discover which genes Foxn1 affected; these included genes responsible for creating and selecting specialized T cells that keep a person healthy.

Improving elderly health

The findings of the study give researchers a better idea of which genetic factors affect the immune system. Having this knowledge, they say, will eventually contribute towards helping elderly people stay healthier for longer.

“The findings from these studies . . . provide important insight into the genetic control of regular TEC function and identify new potential strategies to preserve thymus function with age, raising the prospect of a healthier old age,” explains Professor Georg Hollander of the University of Oxford’s Department of Pediatrics.

The full study has been published in the journal Nature Immunology.


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