Murine malaria: resistance of AXB/BXA recombinant inbred mice to Plasmodium chabaudi

Abstract

The level of resistance to infection with Plasmodium chabaudi is genetically controlled. We have previously reported that a single dominant gene is responsible for the variation in host resistance to malaria between susceptible A/J- and resistant C57BL-derived mice. In the present study, recombinant inbred strain analysis was performed with AXB/BXA recombinant inbred strains derived from A/J and C57BL/6 progenitors. Typing of 17 AXB/BXA recombinant inbred strains confirmed the unigenic control of inheritance in this particular strain combination and allowed us to demonstrate genetic linkage between the traits of resistance (defined as a prolonged survival and a low peak parasitemia) and the magnitude of splenomegaly. The influence of sex on the course of infection, which we previously reported in the examination of segregating populations (Stevenson et al., Infect. Immun. 38:80-88, 1982), was again demonstrated in the survey of RI strains.

Resistance to Plasmodium chabaudi in B10 mice: influence of the H-2 complex and testosterone

“…Mice with a BALB or DBA background were susceptible, while strains with B10 background were resistant. This indicates that resistance and susceptibility are controlled by a non-H-2 gene(s), which confirms previously presented data (2,15,(39)(40)(41).…”

Human recombinant tumor necrosis factor alpha protects susceptible A/J mice against lethal Plasmodium chabaudi AS infection

“…This observation was initially made in the segregating backcross and hybrid populations derived from resistant C57BL-derived B10.A and susceptible A/J parental mice. We have subsequently confirmed unigenic control of resistance to P. chabaudi AS by typing AXB/BXA recombinant inbred mouse strains derived from progenitor C57BL/6 and A/J mice (25). Susceptible mouse strains, such as A/J, develop a fulminant parasitemia; 100% of the animals succumb to infection, with a mean survival time (MST) of less than 10 days.…”

CD4+ and CD8+ T lymphocytes both contribute to acquired immunity to blood-stage Plasmodium chabaudi AS

“…The results of the experiments presented in this study k* IdI1III1I demonstrate the importance of both CD4+ and CD8+ T lymphocytes in the development of acquired immunity to blood-stage infection with P. chabaudi AS. For these studies, we used C57BL/6 hosts, which we have previously characterized as resistant to infection with this parasite 3 7 9 10 12 16 20 (34)(35)(36). Depletion of T cells, specifically CD4+ T cells, resulted in a significantly higher parasitemia as early as 7 days postinfection.…”

“…During infection with P. chabaudi AS, susceptible A/J mice develop marked anemia that appears to culminate in their death, whereas resistant C57BL/6 mice suffer only mild anemia (34). In addition, P. chabaudi AS-resistant mouse strains, such as C57BL/6, develop marked splenomegaly, a trait which is either identical to or closely linked to that conferred by the gene controlling resistance to infection with this murine hemoprotozoan parasite (35,36). The importance of an architecturally intact spleen in the control and elimination of an acute malaria infection has been well documented (13,27).…”