Cutting edge: immunity and IFN-gamma production during Listeria monocytogenes infection in the absence of T-bet.

Cutting Edge: Immunity and IFN- Production during Listeria monocytogenes Infection in the Absence of T-bet

Early IFN-gamma production and innate immunity during Listeria monocytogenes infection in the absence of NK cells.

NK cells are believed to play a mandatory role during the early phases of Listeria monocytogenes infection by producing IFN-gamma, which is required for the activation of macrophage effector functions. Mice deficient in the common cytokine receptor gamma-chain (gamma(c)-/-), which completely lack NK cells, were used to examine whether NK cells were essential for resistance to Listeria infection...

IL-12 is dispensable for innate and adaptive immunity against low doses of Listeria monocytogenes.

We have studied IL-12p35-deficient (IL-12p35(-/-)) mice to evaluate the role of IL-12 in resistance against Listeria monocytogenes. In the absence of bioactive IL-12p75, mutant mice acquired higher bacterial organ burden than wild-type mice and died during the first week following infection with normally sublethal doses of Listeria. Moreover, blood IFN-gamma levels were strikingly reduced in mu...

Differences in gamma interferon production induced by listeriolysin O and ivanolysin O result in different levels of protective immunity in mice infected with Listeria monocytogenes and Listeria ivanovii.

Two pathogenic species in the genus Listeria, Listeria monocytogenes and Listeria ivanovii, are characterized by the production of hemolysins belonging to cholesterol-dependent cytolysins, listeriolysin O (LLO) and ivanolysin O (ILO), respectively. LLO, produced by L. monocytogenes, is able to induce gamma interferon (IFN-gamma) production and contributes to the generation of Th1-dependent prot...

Either B7-1 or B7-2 is required for Listeria monocytogenes-specific production of gamma interferon and interleukin-2.

Listeria infection results in the induction of gamma interferon (IFN-gamma)-producing T lymphocytes. Blocking of the costimulatory molecule B7 in vivo led to a marked decrease in antigen-specific production of IFN-gamma and interleukin-2 by lymphocytes. Blocking of both B7-1 (CD80) and B7-2 (CD86) was required in order to inhibit cytokine production, indicating that either molecule could act al...