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Genetic control of acquired resistance to visceral leishmaniasis in mice
L J DeTolla1, L H Semprevivo, N C Palczuk
1Department of Zoology and Bureau of Biological Research, Rutgers University, New Brunswick, New Jersey 08903, USA.
Abstract:
A series of H-2 and non-H-2 congenic resistant (CR) strains on a C57BL/10Sn background were infected with 10(7) amastigotes of Leishmania donovani. Non-H-2 congenic strains B10.LP-H-3b and B10.CE(30NX) and (B10.LP-H-3b x B10)F1 hybrids showed a very rapid decrease in liver-parasite burdens beyond day 21. Parasite counts for these strains at day 35 were significantly lower than for all other strains tested. The rapid decrease in parasite numbers, massive lymphocellular infiltration into the liver and strong delayed hypersensitivity reactions to parasite antigens in strains congenic for a portion of chromosome 2 indicated that acquired immunity to L. donovani was controlled by a dominant gene at or near the Ir-2 locus. In addition, B10.129(10M) mice, which differ from C57BL/10Sn at the H-11 locus, showed highly significant increases in parasite numbers at day 35. Other observations supporting the absence of acquired immunity in B10.129(10M) included negative delayed hypersensitivity tests to parasite antigens and the absence of lymphocellular infiltrate into the liver. Although the differences were not as pronounced, H-2 CR strains with H-2b, H-2a, and H-2k haplotypes also showed significantly greater decreases in parasite numbers by day 35 as compared to other H-2 CR strains.
Insights
A gene near the Ir-2 locus on chromosome 2 controls acquired immunity to Leishmania donovani infection. This gene significantly impacts parasite clearance and immune responses in mice.
Area of Science:
- Immunology
- Parasitology
- Genetics
Background:
- Leishmania donovani is a parasite that causes visceral leishmaniasis.
- Congenic resistant (CR) mouse strains are used to study host-parasite interactions.
- Genetic control of acquired immunity to parasitic infections is complex.
Purpose of the Study:
- To investigate the genetic basis of acquired immunity to Leishmania donovani.
- To identify specific genes or loci controlling resistance and susceptibility to infection.
Main Methods:
- Infection of various H-2 and non-H-2 congenic resistant mouse strains with Leishmania donovani amastigotes.
- Quantification of liver parasite burdens at different time points post-infection.
- Assessment of delayed hypersensitivity reactions and hepatic lymphocellular infiltration.
Main Results:
- Non-H-2 congenic strains with chromosome 2 segments near the Ir-2 locus showed rapid parasite clearance and strong immune responses.
- Mice differing at the H-11 locus (B10.129(10M)) exhibited increased parasite burdens and lacked acquired immunity.
- H-2 congenic strains with specific haplotypes (H-2b, H-2a, H-2k) demonstrated enhanced parasite reduction compared to others.
Conclusions:
- A dominant gene, likely at or near the Ir-2 locus on chromosome 2, controls acquired immunity to Leishmania donovani.
- The H-11 locus may also play a role in modulating susceptibility to L. donovani infection.
- Genetic background significantly influences the development of protective immunity against visceral leishmaniasis.
