One of the specific hypotheses for the association of worms with protection from severe malaria was that worms led to an increase in IgE complexes that activated the FCεRII (CD23) and thereby releases the anti-inflammatory IL10 and activated the inducible Nitric oxide synthase, which led to the release of nitric oxide, and reduced sequestration of parasitized red blood cells [40]. Here, FCER2 is linked to malaria.