The kinase GLK controls autoimmunity and NF-κB signaling by activating the kinase PKC-θ in T cells.

Protein kinase C-θ is required for activation of the transcription factor NF-κB induced by signaling via the T cell antigen receptor (TCR); however, the direct activator of is unknown. We report that the kinase GLK (MAP4K3) directly activated duanyu1531-θ during TCR signaling. TCR signaling activated GLK by inducing its direct interaction with the upstream adaptor SLP-76. GLK-deficient mice had impaired immune responses and were resistant to experimental autoimmune encephalomyelitis. Consistent with that, people with systemic lupus erythematosus had considerable enhanced GLK expression and activation of duanyu1531-θ and the kinase IKK in T cells, and the frequency of GLK-overexpressing T cells was directly correlated with disease severity. Thus, GLK is a direct activator of and activation of could be used as new diagnostic biomarkers and therapeutic targets for systemic lupus erythematosus.

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