Monocytes heterozygous for the Asp299Gly and Thr399Ile mutations in the Toll-like receptor 4 gene show no deficit in lipopolysaccharide signalling.

It is possible, for example, that efficient recognition of Gram-negative heat shock proteins may be significant in combatting infection and it has already been shown that recognition of human heat shock proteins has a role to play in atherogenesis ( 23 ).

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