The hotter our body temperature, the more our bodies speed up a key defence system that fights tumours, wounds or infections, according to a study.
This new understanding could lead to more effective and fast-working drugs which target a key protein involved in this process.
Biologists from the Universities of Warwick and Manchester in the UK found that inflammatory signals activate 'Nuclear Factor kappa B' (NF-?B) proteins to start a 'clock' ticking.
In the clock, NF-?B proteins move backwards and forwards into and out of the cell nucleus, where they switch genes on and off, researchers said.
This allows cells to respond to a tumour, wound or infection, they said.
When NF-?B is uncontrolled, it is associated with inflammatory diseases, such as Crohn's disease, psoriasis and rheumatoid arthritis.
At a body temperature of 34 degrees, the NF-?B clock slows down. At higher temperatures than the normal 37 degree body temperature, such as in fever or 40 degrees, the NF-?B clock speeds up.
The researchers predicted that a protein called A20 - which is essential to avoid inflammatory disease - might be critically involved in this process.
They then removed A20 from cells and found that the NF-kB clock lost its sensitivity to increases in temperature.
David Rand, a professor at the University of Warwick, explained that in normal life the 24 hour body clock controls small (1.5 degree) changes in body temperature.
"The lower body temperature during sleep might provide a fascinating explanation into how shift work, jet lag or sleep disorders cause increased inflammatory disease," Rand said.
"This is a good example of how mathematical modelling of cells can lead to useful new biological understanding," said Dan Woodcock from the University of Warwick.
While the activities of many NF-kB controlled genes were not affected by temperature, a key group of genes showed altered profiles at the different temperatures.
These temperature sensitive genes included key inflammatory regulators and controllers of cell communication that can alter cell responses.
(This story has not been edited by Business Standard staff and is auto-generated from a syndicated feed.)