A. Poltorak is the first-listed author of a1998 study connecting altered lipopolysaccharide responses in two mouse strains to mutations in the mouse Tlr4 gene. The gene encodes Toll-like receptor 4, a component of the host response to bacterial material. The verified indexed byline is A. Poltorak; no expanded given name is inferred here.[ref]
Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 gene by A. Poltorak and others. Science282,2085–2088; indexed byline and Abstract
The comparison made two forms of evidence meet. The
C3H/HeJ strain had an altered coding sequence, whereas C57BL/10ScCr had a mutation eliminating normal receptor function. Both had impaired lipopolysaccharide signalling. Their relative resistance to endotoxin accompanied increased susceptibility to Gram-negative bacterial infection.[ref]The contrast is scientifically important: reduced response to a bacterial product is not automatically improved defence against the bacterium. Linking inherited variation to a molecular receptor helps distinguish recognition of a stimulus from the many downstream consequences of an immune response. The study's host-genetic comparison therefore supplied more information than testing whether a purified substance was inflammatory in one uncharacterized animal.
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