The ˜10 members of the Toll-like receptor family trigger the production of inflammatory mediators when microbes are detected by innate immune cells. These signals modulate innate immune defense and are critical for orchestrating adaptive immune activation. Distinct (though overlapping) inflammatory responses are induced to combat different microbes and this specificity is mediated in part by selective adapter signaling molecule usage by the individual TLRs. TLR3 is unique compared to the other TLRs in that it does not utilize the adapter, MyD88. However, this interpretation follows from the measurement of an incomplete set of immune responses to the TLR3 ligand, double-stranded RNA. Interpretation further is complicated by the observation that murine macrophages exhibit heterogeneous cell-cell responses to double-stranded RNA. Using mRNA expression measurements by microarrays, we have characterized the role for different signaling adapters in global expression responses to purified stimuli, and the mechanisms for heterogeneity in single cell responses are being defined.
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