Toll-like receptors (TLRs) are signaling molecules that recognize different microbial products during infection and serve as an important link between the innate and adaptive immune responses (1-3). These proteins act through adaptor molecules such as TIRAP and MyD88 to activate various kinases and transcription factors (4,5). In TIRAP-deficient mice, TLR signaling in response to TLR2 ligands (using either TLR1 and TLR6 as co-receptors) is totally abolished, suggesting that MyD88 and TIRAP work together and are both required for TLR2 signaling (6). Furthermore, these mice are also resistant to the toxic effects of LPS and show defects in NF-κB and MAP kinase activation, suggesting that TIRAP is also involed in TLR4 signaling (6,7)
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