IL33 and cerebral malaria: Our study shows association of admission plasma sST2 levels with neuronal injury and cognitive impairment, and the pathway outlined is consistent with experimental cerebral malaria (ECM) studies in which the IL-33/ST2 pathway initiated oligodendrocyte and microglial responses in early infection, resulting in greater neuroinflammation, neuronal damage, and associated neurological and cognitive deficits [28].