Even though there are indirect epidemiological data suggesting that IgM Ab does not participate in protection [23,24], some evidence suggests a protective role in cases such as: (a) mice with an X-linked recessive B-cell deficiency do not produce IgM and are susceptible to Plasmodium yoelii [24]; (b) the addition of monoclonal IgM Ab to a malaria vaccine, raising its protective properties [25]; (c) the IgM level, which correlated with a decrease of the parasitaemia in individuals living in an area of hyperendemic malaria [26]. Here, CD40LG is linked to B cell deficiency.