TNF and acute kidney injury: During AKI, kidney DCs are activated by binding of TLRs and NLRs to cell debris and other DAMPs, thus increasing the expression of costimulatory molecules and proinflammatory cytokines such as tumor necrosis factor α (TNF-α) and antigen presentation to T cells in draining lymph nodes (Dong et al., 2007; Snelgrove et al., 2017), thus contributing to T-cell–mediated inflammation.