In KCs, SIRT1 deacetylates the NF-B p65 subunit, inhibiting its transcriptional activity and reducing the expression of pro-inflammatory cytokines such as TNF-, IL-1, and IL-6
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Interestingly, the lack of change in glycolysis flux in melanocytes interaction with vitiligo skin T cells (via jak/STAT signaling described in Figure 1A) suggests that ROS production (with the extra oxygen consumption) over to ATP production (as illustrated in Figure 2), as discussed in this paper, is a profile to activating cell apoptosis in epidermal from vitiligo patients
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