Figure 2. Signaling pathways from mammalian TLRs. A) A general signaling pathway emanating from MyD88, Engagement of the TLRs leads to recruitment or the adaptor MyD88 and activation or the IRAK family of kinases, Phosphorylated IRAK then dissociates from the receptor complex and activates TRAF6, which becomes ubi qui tin a led and activates TAB-l/TAR-2/TAK-l, TAK-I subsequently triggers both the MAP kinase pathway, and degradation of I KB with subsequent translocation of NF-kB to the nucleus. Activation of this pathway leads to induction or genes for inflammatory cytokines like TNFci, and maturation of DCs, B) Diversity of TLR signaling. MyD88 is essential Tor signaling through most of the TLRs, but an additional adaptor, TIR APT is involved in signaling by TLR2/1/6 and by TLR4. 3ELR4 and TLR3 also signal independently of MyD88 in pathways leading to delayed activation of NF-kB, and activation of another transcription factor, lliF-3. the MyD88 independent signaling results in upregulation of co-stimulatory molecules on DCs and induction of genes such as IFNfJ and IP-JO.

There are several controversial reports addressing the Specificity of recognition by the mammalian TLRs, which is not surprising considering the relative purity of components that are isolated from microbial systems. Chemical synthesis is thus the safest way to go, and this has been done for some of the TI.R ligands. However, this is also the joy of this field right now: We are becoming aware that TLRs can discriminate between subtle structural differences in complex molecules, thus imparting specificity to innate immunity.

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