The findings may be used to develop methods to shut down uncontrolled inflammation, restore immune system regulation, and treat chronic autoimmune disorders such as lupus.
The research was led by Greg Lemke, PhD, professor of Molecular Neurobiology at the Salk Institute and he was funded by the Lupus Research Institute (LRI).
By autoimmunity, it is meant that the immune system which is designed to repel outside invaders by mistake builds up an incontrollable destructive inflammatory attack against the bodys own tissues and organs.
We have found an essential switch that controls immune inflammation, said Dr Lemke.
In this study, Dr. Lemke mounts on findings that he and his team previously reported, when he noticed that mice genetically engineered to be born without a tiny family of three receptors TAM receptor tyrosine kinases eveloped an autoimmune illness similar to lupus in humans.
Dr. Lemke illustrated how under normal circumstances, these TAM receptors, are pivotal in stopping the immune system from building up an incontrollable inflammatory response against invading viruses and bacteria.
He also explained that when immune cells are prompted by chemical messengers (cytokines) to attack, they also activate TAM receptors, which then alert the cells to no longer react to the cytokines. This keeps the immune system orderly as well as relatively quiet.
However, in people with lupus and certain other autoimmune illnesses, the TAM signalling network may be seriously compromised.
The switch to restrain inflammation on this network may be absent thus resulting in immune system chaos.
Those who are affected by lupus tend to have low levels of a blood factor (proteins S) that TAM receptors require to carry out their job.
Administering modified versions of protein S, or its related TAM activator Gas6, to people with lupus may signify a way of stopping the immune system destruction of precious organs and tissues.
This is definitely something we intend to investigate, said Dr. Lemke.
This finding is reported in the recent issue of the journal Cell. (ANI)