diapedese

Diapedesis, commonly referred to as leukocyte extravasation, is the process by which white blood cells move out of the bloodstream and cross the endothelial lining of vessels to reach tissues. It is central to inflammatory responses and immune surveillance.

During diapedesis, leukocytes first margin along the endothelium and roll on its surface via selectin molecules. Chemokines activate the leukocytes, promoting firm adhesion through integrins such as LFA-1 binding to ICAM-1 and VCAM-1. The final step, transmigration, involves crossing the endothelial barrier and occurs via two main routes: paracellular migration between adjacent endothelial cells and transcellular migration directly through an endothelial cell. Endothelial junctional proteins such as PECAM-1 (CD31), JAMs, and VE-cadherin coordinate junction opening and cytoskeletal remodeling to permit passage.

The process is tightly regulated in time and space and typically favors neutrophils early in acute inflammation, followed by monocytes and lymphocytes as the response evolves. Chemokines, cytokines, and hemodynamic forces shape the magnitude and direction of diapedesis.

Clinically, diapedesis is essential for effective host defense against infections but can contribute to tissue damage when excessive or chronic, as in autoimmune diseases. Pathological enhancement of diapedesis is also implicated in cancer metastasis, where tumor cells exploit similar endothelial traversal mechanisms. Therapeutic strategies targeting adhesion molecules or chemokine signaling are explored to modulate inflammatory responses.

The term diapedesis derives from Greek, roughly meaning “to walk or leap through,” reflecting the movement of leukocytes through the vessel wall. The concept has been described since the 19th century as part of studies on inflammation.