Abstract
Malaria caused by the Plasmodium falciparum strain is more severe because of this protozoan's ability to disrupt the physiology of host cells during the blood stages of development by initiating the production of the interleukin-10 (IL-10) family of cytokines. P. falciparum feeds on hemoglobin and causes host cells to adhere to the walls of blood vessels by remodeling their composition. IL-10 is produced by CD4+ T cells that inhibits antigen-presenting cells' activity to prevent inflammation. This cytokine and its family members are crucial in promoting malarial infection by inhibiting the host's protective immune response, thus initiating Plasmodium parasitemia. IL-10 is also responsible for preventing severe pathology during Plasmodium infection and initiates several signaling pathways to alter the physiology of host cells during malarial infection. This review summarizes the critical aspects of P. falciparum infection, including its role in signaling pathways for cytokine exudation, its effect on microRNA, the human immune response in malaria, and the role played by the liver hormone hepcidin. Moreover, future aspects of vaccine development and therapeutic strategies to combat P. falciparum infections are also discussed in detail.