TLR 11 belongs to the Toll-like receptor (TLR) family and the Interleukin-1 receptor/Toll-like receptor superfamily. By recognizing molecular patterns present on microbes, it helps propagate a host immune response. TLR 11 plays a fundamental role in both the innate and adaptive immune responses, through the activation of Tumor necrosis factor-alpha, the Interleukin 12 (IL-12) response, and Interferon-gamma (IFN-gamma) secretion. TLR 11 specifically mounts an immune response to two different microbes: Toxoplasma gondii (T. gondii) and uropathogenic Escherichia coli (E. coli). Placental alkaline phosphatase is one of the most stable isoenzyme, only existing in the placenta of higher primates. These characteristics make placental alkaline phosphatase suitable to use as a reporter gene for the analysis of promoter activity and gene expression in cell culture and animal serum. The natural form of placental alkaline phosphatase (PLAP) is membrane anchored. The recombinant form of placental alkaline phosphatase (secreted alkaline phosphatase, SEAP) is used for reporter gene function. SEAP is created by inserting a translational terminator after amino acid 489 (Berger, et al., Gene 66 : 10. This mutation converts the membrane-bound PLAP protein into the secreted protein. As a major transcription factor, NF-kB plays a key role in regulating genes responsible for the innate and adaptive immune responses. In unstimulated cells, the NF-kB dimers are held in the cytoplasm by IkBs that masks the nuclear localization signals of NF-kB. Upon cell stimulation, which leads to IkB degradation, NF-kB quickly translocates to the nucleus and activates various genes that have DNA-binding sites for NF-kB.