How Immune Cells Trigger Inflammatory Responses?

In a discovery that may pave the way for new treatments for many human diseases including cancer, scientists have identified how the immune cells' are triggered for inflammatory responses. Immune cells play an essential role in the maintenance and repair of our bodies. When human body gets injured, the immune cells mount a rapid inflammatory response to protect against infection and helps in healing of the damaged tissue.

"While this immune response is beneficial for human health, many human diseases (including atheroscelerosis, cancer and arthritis) are caused or aggravated by an overzealous immune response," said lead researcher Helen Weavers from University of Bristol in Britain. The findings showed that immune cells get 'activated' by eating a dying neighbouring cell before they are able to respond to wounds or infection.

In this way, they build up a molecular memory of this meal, which shapes their inflammatory behaviour. Then ingestion of this dying cell activates the damage signalling via a calcium flash, which leads to an increase in the amount of an important damage receptor in the immune cell.

High levels of this receptor then enables the immune cell to sense the damage signals that entice them towards a wound during inflammation. Without this signalling the cells are blind to wounds and infections.

The study is a major step towards finding novel ways to clinically manipulate immune cells away from sites of the body where they are causing the most damage. For the research, published in the journal Cell, the team used Drosophila melanogaster -- the fruit fly -- to study how the macrophage -- immune cell -- becomes activated in order to respond to injury or infection.

"This is an exciting advance in our understanding of immune cell behaviour, and takes us a step closer to designing novel therapeutic ways to influence immune cell behaviour within patients in the clinic," said Will Wood, professor and senior research fellow at Wellcome Trust in Britain.

Source-IANS