Figure 1.

Protective type 2 mechanisms against helminth parasites in the skin. In primary infection (left), N. brasiliensis larvae are quickly attacked by neutrophils, releasing extracellular traps (NETs); however, parasite DNases can break down the NETS, allowing helminths to continue their systemic migration. In secondary infection with the same parasite (center), IgE-armed basophils release IL-4 to activate M2 macrophages (shown in green), swarming around the larvae and upregulating Arg1, which deprives parasites of an essential amino acid. Whether Arg1 actually exits the cell is not known. In infections with S. stercoralis, basophils are not required, but a combination of eosinophils and neutrophils can trap larvae in the skin through a combination of NETs and eosinophil extracellular traps (EETs), and the release of noxious products myelin basic protein (MBP, from eosinophils) and myeloperoxidase (MPO, from neutrophils).