Pre‐erythrocytic stages of plasmodia. Role of specific and nonspecific factors

Abstract

Protection against pre-erythrocytic stages of malaria is possible as demonstrated by the generation of resistance after immunization with irradiated sporozoites. However, mechanisms involved are more numerous and intricate than previously believed and it progressively appears that the role of the presumed target, the sporozoite, might be negligible compared with that of the hepatic stage. The comparative use of in vivo and in vitro models clearly demonstrates that the intrahepatocytic parasite can be the target of antibodies, cytokines, phagocytic and cytotoxic cells, nonspecific factors--mechanisms in part induced by the previous or subsequent developmental stages.

Liver CD4−CD8− NK1.1+ TCRαβ Intermediate Cells Increase During Experimental Malaria Infection and Are Able to Exhibit Inhibitory Activity Against the Parasite Liver Stage In Vitro

“…However, the expression of Fas molecules by infected hepatocytes remains to be demonstrated. On the other hand, cytokines are known to have an important role as mediators and effectors in the host response to plasmodial infection (55). So, the partial but significant reduction by the anti-IFN-␥ Ab of the inhibition of P. yoelii intrahepatocytic schizogony induced by parasiteprimed NK1.1 ϩ TCR␣␤ ϩ liver cells also suggests that IFN-␥ may be produced by these iHLs themselves and play a role in their inhibitory activity (34).…”

Survival and antigenic profile of irradiated malarial sporozoites in infected liver cells

“…The mechanism of protection was thought to be mediated primarily by antibodies directed against the circumsporozoite proteins (CSP). Although such antibodies can neutralize sporozoite infectivity (20,26) and high anti-CSP titers can protect humans against a sporozoite challenge (16), it is now thought that a major component of the protective response generated by irradiated sporozoite is mediated by CD8+ (cytotoxic) T cells directed at the liver or exoerythrocytic (EE) stage (17,33,47). Intrahepatic CSP (20, 39) is thought to be processed (44) by the hepatocyte and presented as a target for protective CD8+ T cells in rodents (31,32), and circumstantial evidence suggests that this is also true in humans (18,24).…”

Vaccination trial against canine visceral leishmaniasis

“…In this respect it is worth mentioning that immune modulation mediated by anti-viral and anti-parasite antibodies may lead to opposite effects: neutralization or enhancement (Halstead, Portefield & O'Roville 1980, Kasper, Currie & Bradley 1985, Mendis et af. 1987, Mazier et al 1989. In experimental cutaneous leishmaniasis, some immunization regimens based on killed parasites may also result in disease exacerbation, the mechanisms of which are related to the production of a diseasepromoting population of CD4+ T-lymphocytes (Titus et al 1984, Liew et al 1985, Milon et af.…”