= A. Poltorak
{c}
<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.<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]{ref}
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.<Defective LPS signaling in C3H HeJ and C57BL 10ScCr mice: mutations in Tlr4 gene by A. Poltorak and others>[Abstract, strain-specific Tlr4 mutations and contrasting phenotypes]{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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