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CUTTING EDGE |
Responses During Viral Infection1
*
Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, RI 02912;
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115; and
Department of Host Defense Research, Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan
Optimal protective effects for defense against infection require
orchestration of immune responses spanning multiple host compartments
and divergent local regulation at particular sites. During murine
cytomegalovirus infections known to target spleen and liver,
IL-12-induced IFN-
from NK cells is crucial for resistance. However,
the roles for IL-18 and/or IL-12 in regulating hepatic IFN-
responses, as compared with systemic or splenic responses, have not
been defined. In this report, mice genetically deficient in either
IL-18 or IL-12p35 exhibited up to 95% reductions in systemic and
splenic IFN- responses. Surprisingly, IFN- responses were
preserved in the livers of IL-18-deficient, but not IL-12p35-deficient,
mice. Cytokine requirements for host survival also differed. Under
conditions where mice lacking IL-12p35 exhibited 100% mortality, those
lacking IL-18 survived. Taken together, our results delineate
contrasting compartmental requirements for IL-18 and suggest that
preservation of local, hepatic IFN- production is critical for host
defense during murine cytomegalovirus
challenge.
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