01841nas a2200337   4500000000100000008004100001260001300042653001200055653001400067653002100081653001200102653001600114653000900130653002600139653002900165653002400194653002400218653001700242653002600259653002800285100001400313700001300327700001300340700001600353700001300369245007100382300001000453490000700463520101900470022001401489       2002                            d  c2002 May10aAnimals10aGranuloma10aInterferon-gamma10aleprosy10aMacrophages10aMice10aModels, Immunological10aMycobacterium Infections10aMycobacterium avium10aMycobacterium bovis10aNitric Oxide10aNitric Oxide Synthase10aTuberculosis, Pulmonary1 aCooper AM1 aAdams LW1 aDalton D1 aAppelberg R1 aEhlers S00aIFN-gamma and NO in mycobacterial disease: new jobs for old hands.  a221-60 v103 a<p>Granulomatous disease following exposure to Mycobacterium tuberculosis, Mycobacterium leprae or Mycobacterium avium is correlated with strong inflammatory and protective responses. The mouse model of mycobacterial infection provides an excellent tool with which to examine the inter-relationship between protective cell-mediated immunity and tissue-damaging hypersensitivity. It is well established that T cells and interferon (IFN)-gamma are necessary components of anti-bacterial protection. We propose that IFN-gamma also modulates the local cellular response by downregulating lymphocyte activation and by driving T cells into apoptosis, and that the events that limit excessive inflammation are largely mediated by IFN-gamma-induced nitric oxide (NO). In several murine models of mycobacterial infection, the absence of IFN-gamma and/or NO results in dysregulated granuloma formation and increased lymphocytic responses, which, in the case of M. avium infection, even leads to reduced bacterial growth.</p>  a0966-842X