TNF and acute kidney injury: In AKI, renal DCs are activated by binding to cell debris and other mediators through TLRs and NLRs, leading to increased expression of co‐stimulatory molecules and pro‐inflammatory cytokines (e.g., TNFα) and presenting antigens to NK T cells in draining lymph nodes, thus promoting NK T cell‐mediated inflammation.[79, 80] Blocking the interaction between renal DCs and NK T cells and inhibiting IRI‐induced renal inflammation and NK T cell activation can protect the kidneys from IRI.