Toll-like receptor 5 (TLR5) participates in the innate immune response to microbial agents. TLR5 mediates detection of bacterial flagellins. TLR5 acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Individuals with a common stop codon polymorphism in position 392 are unable to mediate flagellin signaling. This polymorphism acts in a dominant fashion and is associated with susceptibility to pneumonia caused by Legionella pneumophila. Genetic variations in TLR5 are associated with resistance to systemic lupus erythematosus type 1 (SLEB1). Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a comple, Xenopus/Amphibian, genetic basis.