Calcium signaling helps immune cells spread
Neutrophils are immune cells that travel through tissues to fight infections. Their ability to reach sites of infection depends on cell movement and dynamic changes in the cell’s internal skeleton, in particular structures made up of actin fibers. Calcium signaling is known to play a role in coordinating this activity, but the mechanisms involved have remained unclear.
Investigating the role of Stim1 and Stim2
In a , researchers from the laboratory of Prof. Nicolas Demaurex investigated whether specific calcium-regulating proteins - Stim1 and Stim2 - influence neutrophil spreading and movement. The team found that neutrophils lacking Stim1 and 2 failed to increase calcium signals upon adhesion, resulting in reduced actin fiber formation, impaired spreading and slower movement.
Compared to normal neutrophils (left film), neutrophils lacking Stim1/2 (right film) move more slowly and have a default in actin formation (pink to yellow color).
Potential implications
These findings suggest that Stim1 and Stim2 are involved in the remodelling of the actin skeleton necessary for proper neutrophil spreading. This work adds a new level of understanding to how neutrophils function during immune responses and how calcium dynamics control immune cell movement.