Parasitic and helminthic infections drive the immune system towards TH2 cytokine production and concurrent eosinophilia. Since eosinophil infiltration in infected organs and skin is a common finding, eosinophils are thought to have a specific role in parasite killing [127] . Although, a challenged theory; the deposition of the cytotoxic protein ECP could be a mechanism by which the immune system kills off the intruders. Indeed, the eosinophilia in parasitic diseases is associated with elevated ECP in circulation (table 1) [72, 128] . ECP is also found released from eosinophils in proximity to parasites in skin and lymph nodes [129, 130] . The ability for ECP to kill or paralyse parasites and helminths have been analysed in vitro and high quantities were needed to influence the organisms. Three-hr-old larvae of Schistosoma mansoni were incubated with 10 μM (190 μg/mL) ECP and 60 percent were killed. S. mansoni, 3 days of age, were paralysed by the protein [131] while 50 μM (950 μg/mL) ECP killed 40 percent of Trypanosoma cruzi by 6 hr and 90 percent of Brugia malayi by 48 hr. This cytotoxicity of ECP to parasites was inhibited by heparin [132] and dextran sulphate, probably by interfering with the tryptophan and arginine residues as discussed earlier.