Tehran University of Medical Sciences Iranian Journal of Parasitology 1735-7020 10 4 2015 12 14 638 647 EN Hanaa BAKIR Department of Parasitology, Faculty of Medicine, Assiut University, Assiut, Egypt Doaa YONES Department of Parasitology, Faculty of Medicine, Assiut University, Assiut, Egypt Lamia GALAL Department of Parasitology, Faculty of Medicine, Assiut University, Assiut, Egypt Enas HUSEEIN Department of Parasitology, Faculty of Medicine, Assiut University, Assiut, Egypt 2015 12 14 2015 12 14 Background: In an effort to understand what limits the virulence of malaria para­sites in relation to the host genetic and immunogenic background, we investi­gated the possibility that the parasite and host genotype crossover interac­tions constrain virulence. Methods: Two groups of mice from different genotypes were used (C57BL/6 (B6) and DBA/2 mice). The mice were infected with a virulent parasite line Plasmo­dium yoelii17XL (P. yoelii17XL). Parasitemia, hematocrit value and lympho­cytes yielded by livers and spleens were evaluated. Fluorescence Activated Cell Sorting (FACS) analysis illustrated phenotypic characterization of lymphocytes. Results: Infection with P. yoelii17XL did not result in thedeath of DBA/2 mice. In contrast,B6 mice developed significantly high parasitemia and succumbed to death. Using (FACS) analysis, DBA/2 mice were found to experience a marked expansion of interleukin (IL)-2Rb+ CD3int cells and gd T cells in the liver, espe­cially in the recovery phase. The expansion of unconventional T cells (i.e. B220+ T cells) was also marked in DBA/2 mice. Conclusion: The outcome of murine malaria infections depends on the dynamic interplay between the immune-mediator and the genotype of the host. https://ijpa.tums.ac.ir/index.php/ijpa/article/view/666 https://ijpa.tums.ac.ir/index.php/ijpa/article/download/666/547