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• W2034831375 abstract "Interleukin-12 is a potent activator and initiator of type-1 T cell development, and can be used as an adjuvant to bias for the development of vaccine-induced Th1 immune responses. During vaccination of MHC class I deficient beta-2 microglobulin knockout mice (β2M(-/-)) with an IL-12/αIL-4 Th1 biasing procedure, all of the mice died. None of the IL-12/αIL-4 treated wild type mice developed any noticeable complications. We hypothesized that NK cells may be activated by IL-12 treatment in these β2M(-/-) mice, leading to necrosis and eventual death. IL-12/αIL-4 treatment of β2M(-/-) mice resulted in increased NK cell numbers and activation status (IFN-γ(+), CD69(+)). Finally, in vivo depletion of NK cells reversed the pathology induced by IL-12/αIL-4 treatment in β2M deficient mice. These results indicate that IL-12 combined with αIL-4 irreversibly activates NK cells leading to a disseminated inflammatory pathology and death in β2M(-/-) mice." @default.
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• W2034831375 date "2013-10-01" @default.
• W2034831375 modified "2023-09-24" @default.
• W2034831375 title "Lethal NK-mediated inflammation induced by IL-12 in the absence of polymorphic and nonpolymorphic MHC class I molecules" @default.
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• W2034831375 doi "https://doi.org/10.1016/j.cyto.2013.06.320" @default.
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