IndraLab

"This immunological response is explained by the impairment of STAT4 phosphorylation and IFN-γ production as the result of STAT1 hyperactivation.11 Another group of researchers attributed the susceptibility of Usp18lty9 mice to S. typhimurium or Mycobacterium tuberculosis infection to elevated levels of IL-10, IL-1β, or IL-17, in addition to the deregulation of autophagy markers.10 Surprisingly, the contradictory nature of these two results obtained with Usp18 knockout mice and Usp18lty9 mice can be explained by either the different backgrounds of the mice or the specific ENU-induced mutation of Usp18."