In patients with leukocyte adhesion deficiency (LAD), which function remains intact despite the defect?

In leukocyte adhesion deficiency (LAD), a primary defect occurs in the ability of leukocytes to adhere to blood vessel endothelium, which is crucial for their migration into tissues during an immune response. This defect is primarily caused by mutations affecting the integrins on the surface of leukocytes.

While phagocytosis, chemotaxis, and margination are all processes that are significantly affected by this adhesion defect, antibacterial activity, or bacterial killing, remains largely intact. This is because once leukocytes are in the site of infection, they can still use their intracellular mechanisms to kill bacteria. The problem primarily arises during the initial steps of the immune response—when leukocytes attempt to exit the bloodstream and reach the site of infection.

Thus, despite the difficulties faced in adhering and migrating to areas of infection due to the defect, the actual process of killing bacteria is still functional, allowing for some level of immune response to continue. This distinction highlights that LAD primarily affects the movement and localization of immune cells rather than their innate ability to eliminate pathogens once they are present in tissues.