Resveratrol protects us from rogue or infected cells by stimulating perforin – the powerful bullet of our immune system

The human immune system's assassin is a protein called perforin. Perforin punches holes in rogue cells. Recently a joint team from the UK and Australia viewed perforin in action through a powerful microscope for the first time. According to Professor Helen Saibil, who leads the UK team "Perforin is a powerful bullet in the arsenal of our immune system -- without it we could not deal with the thousands of rogue cells that turn up in our bodies through our lives." "Perforin is our body's weapon of cleansing and death," said Professor James Whisstock from Monash University, Melbourne, project leader for the Australian segment of the team.

Perforin works by punching holes in cells that have become cancerous or have been invaded by viruses. The holes let toxic enzymes into the cells, which then destroy them.

If perforin isn't working properly the body can't fight infected cells. And there is evidence from mouse studies that defective perforin leads to an upsurge in malignancy, particularly leukemia, so says Professor Joe Trapani, head of the Cancer Immunology Program at the Peter MacCallum Cancer Centre in Melbourne, Australia.

The first observations that the human immune system could punch holes in target cells was made by the Nobel Laureate Jules Bordet over 110 years ago, but we have had to wait for the latest advances in structural molecular biology to find out how exactly this happens

Recently scientists from the Department of Physiology, College of Medicine, Chang Gung University, Taiwan found that supplementing rats with Resveratrol improved the functionality of their natural killer cells (NK cells); immune cells that are a first line of defense against tumor cells and cells infected with viruses. In investigating isolated cells they also found that the greater the concentration of Resveratrol the higher the activity of NK cells. It turns out that Resveratrol works by stimulating the activity of perforin. The research is published in the May 2010 issue of the Journal of Cellular Physiology