One prominent role of NK cells lies in the detection and destruction of abnormally modified cells for instance resulting from viral infections or transforming processes. The recognition of those aberrant cells is facilitated by multiple NK cell specific surface receptors.
By applying Bcl10-, Malt1- as well as Carma1- deficient mice we could show that similar to TCR- and BCR-relayed signaling the ITAM-coupled NK cell receptors NK1.1, Ly49D and NKG2D engage the Bcl10/Malt1/Carma1 complex to activate the transcription factor NF-κB and MAP-Kinases for cytokine production.
Further experiments demonstrated, that in the case of MCMV infection, NK cell proliferation and cytotoxicity were induced in a Bcl10-independent manner, indicating that these two cellular processes are not coupled to cytokine production per se.
Additionally, no significant differences between wild type and Bcl10-deficient mice were observed in terms of the overall survival and the detectable viral load early after MCMV infection. Thus, the cytokine production does not seem to be essential for the primary defense to occur against Herpes family viruses.
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One prominent role of NK cells lies in the detection and destruction of abnormally modified cells for instance resulting from viral infections or transforming processes. The recognition of those aberrant cells is facilitated by multiple NK cell specific surface receptors.
By applying Bcl10-, Malt1- as well as Carma1- deficient mice we could show that similar to TCR- and BCR-relayed signaling the ITAM-coupled NK cell receptors NK1.1, Ly49D and NKG2D engage the Bcl10/Malt1/Carma1 complex to act...
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