| abstract |
The present invention demonstrates the important role of C/EBP ε in innate immune response against pathogens. Specifically, the inventors showed that in the absence of functional C/EBP ε , mice are severely impaired in their ability to clear S. aureus infection. Neutrophils are particularly affected, and susceptibility to S. aureus can be rectified by treatment with interferon-gamma (IFN-γ). Importantly, increased activity of C/EBP ε , either by induced overexpression of C/EBPE or by application of nicotinamide or an analog, derivative or salt thereof, dramatically enhances immune killing of S. aureus and leads to amelioration of infection. |