Which defect is associated with leukocyte adhesion deficiency (LAD) type 2?

Leukocyte adhesion deficiency (LAD) type 2 is specifically associated with defects in fucosylation that lead to abnormalities in the expression of selectin ligands. The problem arises from the inability to properly fucosylate carbohydrates on the leukocyte surface, which leads to a defect in the synthesis of the sialyl-Lewis x (sLEX) carbohydrate epitope. This epitope is crucial for the binding of leukocytes to endothelium during the process of extravasation, which is essential for an effective immune response. Without functional sLEX, leukocytes cannot adhere properly to the endothelial cells, resulting in impaired migration to sites of inflammation or infection.

In contrast, other choices refer to various components of the immune system that are not directly involved in the specific mechanism of leukocyte adhesion deficiency type 2. For example, the common β chain in CD18 relates to LAD type 1, which affects integrin function, while defects in CD21 and CD95 are related to different immunological conditions that do not affect leukocyte trafficking in the manner described for LAD type 2. Therefore, understanding the role of fucosylation and sLEX in leukocyte function is key to grasping why this option