Other possible mechanisms to modulate the immune system could be induced by the components of bacteria like lipopolysaccharide (LPS), which is derived from the wall of Gram-negative bacteria belonging to Bacteroidetes (this phylum is elevated in the gut microbiota of SLE mice), and thus, through TLR-4 activation, inducing the production of proinflammatory cytokines such as TNF-α, IL-6 and type I interferons (IFN-α, IFN-γ) that are elevated in SLE patients and also in animal models of SLE [36]. The gene discussed is TLR4; the disease is systemic lupus erythematosus.