To test the effects of these metabolites on the innate inflammatory response of the murine RAW 264.7 (RAW) Mɸ cell line, we used heat-killed M. tuberculosis (Mtb), a TLR2 and TLR4 dual-agonist [32], which also is used as an arthritogen in certain animal models of RA [33] and lipopolysaccharide (LPS), a TLR4 agonist, which is a prototypic inducer of innate inflammation. The gene discussed is TLR4; the disease is rheumatoid arthritis.