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Max Planck Institut für Immunbiologie, Freiburg, Germany
Lpsd mouse strains are characterized by
the presence of a defective Lps/tlr4 gene that make them
refractory to the biological activity of LPS. One of the mouse strains
commonly used to study LPS defects is the C57BL/10ScCr (Cr) strain.
However, unlike other Lpsd strains, the Cr
strain also has a heavily impaired IFN-
response to micro-organisms.
As a consequence, unlike other Lpsd mouse
strains, they do not acquire a partial LPS susceptibility when treated
with sensitizing bacteria. Because IL-12 is important for the microbial
induction of IFN-, we investigated whether the production or
function of IL-12 might be defective in Cr mice. IL-12 mRNA (p35 and
p40) was present in the spleen of untreated Cr mice, IL-12p40 mRNA was
inducible in mice injected with live or killed Salmonella
typhimurium, and IL-12 (p70) was inducible in macrophages by
bacteria. Thus, Cr mice exhibit normal IL-12 responses. In functional
tests, splenocytes of untreated or of S.
typhimurium-infected mice failed to produce IFN- when
stimulated with murine rIL-12 or with a combination of IL-12 and murine
rIL-18 or Con A. Furthermore, Cr mice were identical with IL-12p35/p40
and IL-12 receptor 
1 knockout mice in their impaired in
vivo and in vitro IFN- responses to bacteria. Thus, Cr mice carry a
second genetic defect unrelated to the Lps/tlr4 mutation
that underlies the IL-12 unresponsiveness and contributes to the LPS
resistance and impaired innate immune response in this
strain.
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