NLRC5 and bacterial infectious disease: In LX-2 human hepatic stellate cells, knockdown of Nlrc5 increased NF-κB activation after TNF-α treatment [25], whereas in the human monocytic cell line THP-1, knockdown of Nlrc5 eliminated IL-1β processing in response to bacterial infection and downregulated the poly(I:C)-mediated type I interferon pathway [26, 27]; the same effect was observed in virus-infected human foreskin fibroblasts [28].