Apicomplexan protozoans, such as Plasmodium, Toxoplasma, Babesia, Cryptosporidium, Theileria, and Eimeria, are causative agents to both human and animal parasitic diseases. Among those, Plasmodium infection causes malaria which is one of the most devastating diseases worldwide, and the infection of Toxoplasma causes life-threatening toxoplasmosis in humans and animals. It is well known that Plasmodium and Toxoplasma could actively invade host cells and develops inside parasitophorous vacuole (PV). Both parasites could evade host cells' autonomous immunity by avoiding the fusion of PV with the lysosome, but their survival inside PV of host cells is still largely unknown. In addition, the infection of Plasmodium and Toxoplasma could always persist for months or years, indicating both parasites have developed robust immune escaping strategies. Although antigen variance has been involved in this process, other strategies of both parasites to evade or suppress host immune response remain elusive. In addition, malaria transmission also requires parasites to successfully passage through the vector mosquitoes through escaping or suppressing mosquito immune responses. The advance in the research on the mechanisms of both parasites’ escaping or suppressing host (vector) immune responses will shed new light for us to design strategies to prevent the infection from apicomplexan protozoan.
The goal of this Research Topic is to provide a forum to advance research on the strategies of apicomplexan protozoan to survive in host cells and escape or suppress host immune responses and on the exploration of innovative interventions against diseases caused by those apicomplexan protozoans. We welcome manuscripts in the following subtopics:
1) Host cells' autonomous immune response against apicomplexan protozoan, e.g., the role and underlying mechanism of intracellular complement C3 to limit their survival and development of intracellular malaria parasite or Toxoplasma gondii
2) The strategies of apicomplexan protozoan to escape host cells' autonomous immune response, e.g., Toxoplasma gondii in macrophages resists the IFN-gamma killing
3) Host (vertebrates or vector) protective immune responses against invaded apicomplexan, e.g., the regulatory role of neutrophils, NK/NKT, and γδT cells in the activation of CD4+ T cells against the blood-stage malaria parasite, and novel effectors to limit the development of malaria parasite in mosquitoes
4) Mechanisms of apicomplexan protozoan to escape or suppress host (vertebrates or vector) immune response, e.g., novel strategies of the malaria parasite to suppress CD4+ T cell activation to facilitate its survival
Apicomplexan protozoans, such as Plasmodium, Toxoplasma, Babesia, Cryptosporidium, Theileria, and Eimeria, are causative agents to both human and animal parasitic diseases. Among those, Plasmodium infection causes malaria which is one of the most devastating diseases worldwide, and the infection of Toxoplasma causes life-threatening toxoplasmosis in humans and animals. It is well known that Plasmodium and Toxoplasma could actively invade host cells and develops inside parasitophorous vacuole (PV). Both parasites could evade host cells' autonomous immunity by avoiding the fusion of PV with the lysosome, but their survival inside PV of host cells is still largely unknown. In addition, the infection of Plasmodium and Toxoplasma could always persist for months or years, indicating both parasites have developed robust immune escaping strategies. Although antigen variance has been involved in this process, other strategies of both parasites to evade or suppress host immune response remain elusive. In addition, malaria transmission also requires parasites to successfully passage through the vector mosquitoes through escaping or suppressing mosquito immune responses. The advance in the research on the mechanisms of both parasites’ escaping or suppressing host (vector) immune responses will shed new light for us to design strategies to prevent the infection from apicomplexan protozoan.
The goal of this Research Topic is to provide a forum to advance research on the strategies of apicomplexan protozoan to survive in host cells and escape or suppress host immune responses and on the exploration of innovative interventions against diseases caused by those apicomplexan protozoans. We welcome manuscripts in the following subtopics:
1) Host cells' autonomous immune response against apicomplexan protozoan, e.g., the role and underlying mechanism of intracellular complement C3 to limit their survival and development of intracellular malaria parasite or Toxoplasma gondii
2) The strategies of apicomplexan protozoan to escape host cells' autonomous immune response, e.g., Toxoplasma gondii in macrophages resists the IFN-gamma killing
3) Host (vertebrates or vector) protective immune responses against invaded apicomplexan, e.g., the regulatory role of neutrophils, NK/NKT, and γδT cells in the activation of CD4+ T cells against the blood-stage malaria parasite, and novel effectors to limit the development of malaria parasite in mosquitoes
4) Mechanisms of apicomplexan protozoan to escape or suppress host (vertebrates or vector) immune response, e.g., novel strategies of the malaria parasite to suppress CD4+ T cell activation to facilitate its survival