CD4 and malaria: In both P. falciparum infections and rodent malaria models, severe disease syndromes arise in diverse organs (e.g., brain, lungs, placenta) and appear to result from the combined effect of cytoadherence of parasitised red blood cells (pRBCs) in vascular beds and a strong host pro-inflammatory response mediated by cytokines such as TNF-α [24], LT-α [25], and IFN-γ [26], and effector cells such as CD4 [27], [28] and CD8 T cells [29], [30], natural killer (NK) T cells [31], [32], and NK cells [33].