Host genetic background determines whether IL-18 deficiency results in increased susceptibility or resistance to murine Leishmania major infection.

Authors: Wei, XQ  Niedbala, W  Xu, D  Luo, ZX  Pollock, KG  Brewer, JM 
Citation: Wei XQ, etal., Immunol Lett. 2004 Jun 15;94(1-2):35-7.
Pubmed: (View Article at PubMed) PMID:15234532
DOI: Full-text: DOI:10.1016/j.imlet.2004.04.001

Interleukin-18 (IL-18) plays an important role in innate and acquired immunity. IL-18 gene deficient (IL-18-/-) mice of the 129 x CD1 strain were reported to be more susceptible to Leishmania major infection than the wild-type mice. In contrast IL-18-/- mice of the C57BL/6 background were found to be as resistant as the wild-type (WT) mice. To resolve this discrepancy, IL-18 gene deficiency was introduced by backcrossing on to the highly susceptible BALB/c, or the moderately resistant DBA/1 backgrounds. Here we have demonstrated that BALB/c IL-18-/- mice were more resistant to L. major infection than WT BALB/c mice, whereas DBA/1 IL-18-/- mice were markedly more susceptible than their WT littermates. BALB/c IL-18-/- mice produced less IFNgamma and IL-4, whereas DBA/1 IL-18ko mice produced more IFNgamma and IL-4 than their respective WT controls. These result clearly demonstrate that the role of IL-18 in resistance or susceptibility to L. major is determined by host genetic background.


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CRRD Object Information
CRRD ID: 8655927
Created: 2014-05-23
Species: All species
Last Modified: 2014-05-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.